2. Physiology of Vasopressin Secretion and Thirst

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1 2. Physiology of Vasopressin Secretion and Thirst Gary L. Robertson, MD Jane H. Christensen, MSc, PhD Over the last 4 decades, the development and application of several new tools have expanded and refined the understanding of the anatomy, biochemistry, and physiology of vasopressin and the thirst mechanism. Most important in this regard are the immunoassay methods that permit the hormone to be detected and measured at physiologic levels in plasma and tissue, magnetic resonance imaging (MRI), which makes it possible to visualize the posterior pituitary in vivo, and elucidation of the gene and cellular mechanisms involved in hormone synthesis. New insights have arisen from both basic and clinical investigation and are now linking up in ways that satisfy as well as provoke. This article reviews this progress in the realm of normal function. Anatomy The specialized magnocellular neurons that synthesize and secrete vasopressin into the systemic circulation have now been characterized in more detail ( 1 ). As shown many years ago ( 2 ), the cell bodies (or the soma) of these neurons are located mainly in the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus (see figure 1-1 in Chapter 1 [History] of this issue, for further details). They are remarkably large (20-40 μ m cell body diameter) and few in number, maybe only a few thousand, as compared with all of the other cells in the neurohypophysis. Each of them has 1 long unmyelinated, varicose axon that projects through the diaphragm sella to the posterior pituitary. This axon also has collateral branches, many of which project back to and terminate close to the nucleus, where they may contact lateral cholinergic neurons. In the posterior pituitary, the main axon gives rise to thousands of neurosecretory axon swellings and nerve endings that store many vasopressin-containing dense-core secretory vesicles. These vesicles, each of which contains many thousand vasopressin molecules, release their content into adjacent capillaries by exocytosis in response to calcium influx through voltage-gated channels generated by action potentials propagated down Translational Endocrinology & Metabolism, Volume 3, Number 3,

2 the axons ( 3 ). The dendrites of the magnocellular neurons receive about 10,000 regulating synapses from afferent neurons originating in various parts of the brain ( 1 ). Another set of magnocellular neurons that originate in the SON and PVN and project into the posterior pituitary produces oxytocin ( 1 ). A third population of magnocellular neurons constituting approximately 3% of the total in the normal SON appears to produce vasopressin and oxytocin in a 2:1 proportion within the same cell ( 4, 5 ). Vassopressinergic and oxytocinergic magnocellular neurons are also found in smaller numbers in accessory cell groups arranged around and along the blood vessels between the SON and PVN (eg, in the anterior commissural, periventricular, posterior perifornical, circular, and medial forebrain nuclei) ( 6, 7 ). Besides vasopressin and oxytocin, the magnocellular neurons produce several other peptides, although in much smaller amounts ( 1 ). These are, among many others, corticotropin-releasing hormone (CRH) and cholecystokinin (produced mainly by oxytocinergic neurons), galanin and neuropeptide Y (produced mainly by vasopressinergic neurons), and the opioid peptide dynorphin (produced by both cell types, but particularly by vasopressinergic neurons). Other coproduced peptides include thyrotropinreleasing hormone (TRH) and apelin ( 8 ). Whereas the SON is entirely magnocellular, the PVN is divided into a lateral magnocellular section and a more medial parvocellular section ( 1 ). As their name implies, parvocellular neurons have smaller cell bodies (10-15 μ m) than magnocellular neurons. Moreover, they comprise both neuroendocrine cells and neurons that project to more central brain regions. A subpopulation of the parvocellular neuroendocrine cells consists of vasopressinergic cells that project axons to the median A subpopulation of the eminence, at the base of the brain. Here, the parvocellular neuroen docrine nerve endings release vasopressin into the cells consists of blood vessels of the hypothalamo-pituitary vasopressinergic cells that portal system. In rodents, this release seems project axons to the median to be elicited as a response to experimental eminence, at the base of the manipulations of the hypothalamic-pituitaryadrenal (HPA) axis (eg, adrenalectomy and brain. various types of chronic stress) ( 9 ). Upon release, vasopressin seems to act synergistically with CRH produced by the same cells to bring about release of adrenocorticotropic hormone (ACTH) from the corticotropes of the anterior pituitary, which in turn stimulates cortisol secretion from the adrenal cortex ( 9, 10 ). The precise nature and importance of this synergism is incompletely understood, with most information derived from 28 Translational Endocrinology & Metabolism: Posterior Pituitary Update

3 animal studies. However, it appears to play a minor, nonessential role in potentiating the ACTH response to a variety of stresses in homozygous Brattleboro rats that lack the capacity to produce vasopressin ( ). Another subset of parvocellular neuroendodrine cells also projecting to the median eminence produces TRH, which regulates thyroid-stimulating hormone secretion ( 16 ). As mentioned previously, the PVN further contains interneurons and populations of vasopressinergic and oxytocinergic neurons projecting to many other areas of the brain including the amygdala, hippocampus, striatum, suprachiasmatic nucleus, bed nucleus of stria terminalis, and the brainstem ( 17 ). There, vasopressin and oxytocin are presumed to act as neuromodulators or neurotransmitters, and thereby influence neurotransmission. For example, it has been shown that they modulate neural populations in the central amygdala of rats and thereby may regulate the autonomic expression of fear ( 18 ). The finding that common genetic risk variants in the genes that encode the brain receptors for oxytocin and vasopressin are associated with autism and social behavioral phenotypes in people, and that these risk variants affect the structure and function of key regions for social behavior, including the amygdala, anterior cingulate cortex, and hypothalamus, as shown by neuroimaging studies, suggests that vasopressin or oxytocin play some role in central nervous function. However, the importance of these functions in humans is uncertain because patients with mutations that appear to prevent all synthesis of vasopressin do not exhibit any overt abnormalities other than diabetes insipidus defects (see the article by JH Christensen and GL Robertson [Chapter 3] in this issue). The posterior pituitary and its stalk can now be visualized in vivo by MRI. On T1-weighted images, the gland emits a well circumscribed, highintensity signal that resembles that produced by fat but differs from it on proton density/t2-weighted scans ( 19 ). The origin of this signal in the posterior pituitary is evidenced by its size, shape, and stalk can now be visualized The posterior pituitary and its location within the posterior part of the in vivo by MRI. sella turcica ( Figure 2-1 ). It is easily distinguished from the anterior pituitary, which emits a signal of intermediate intensity similar to that of the pons. This posterior pituitary bright spot is found in 90% to 100% of healthy young adults and children, but its size, shape, and position vary considerably from person to person ( ). It is observed significantly less often in the first year of life ( 22 ) and in the elderly. It is also absent in patients with empty sella, even when their vasopressin secretion is normal. On repeat imaging, the signal has also Physiology of Vasopressin Secretion and Thirst 29

4 FIG 2-1. T-1 weighted, midsaggital magnetic resonance image of healthy, normally hydrated adult. Note the high-intensity signal from the posterior portion of the sella turcica. been observed to appear or disappear over time in about 25% of adults (23). The reason for this temporal variation has not been established and may be due in part to slight differences in the location of the gland relative to the midpoint of multiplanar imaging. However, environmentally induced variations in the rate of vasopressin secretion and synthesis may also contribute, because, during sustained osmotic stimulation in rabbits, the intensity of the posterior pituitary bright spot decreases in parallel with its content of vasopressin-containing neurosecretory granules (24, 25). The same association between increased vasopressin secretion and decreased posterior pituitary bright spot has been observed in patients undergoing renal dialysis (26). However, the exact cellular and biochemical origin of the high-intensity signal is not yet established conclusively. The theory that it arises from phospholipid in neurons or pituicytes (27, 28) would appear to be inconsistent with the failure of fat suppression techniques to diminish the signal (29). An alternative theory, that the signal arises from the vasopressin-neurophysin-copeptin complex, is 30 Translational Endocrinology & Metabolism: Posterior Pituitary Update

5 more consistent with the observations that its intensity correlates inversely with the rate of vasopressin secretion and/or the amount of vasopressin stored in the pituitary. However, these observations are also consistent with the possibility that the signal is generated not by the vasopressin complex itself but by some other neuronal component or activity that changes when the rate of vasopressin synthesis changes in response to secretion of the hormone. In any event, it is clear that loss or absence of the posterior pituitary bright spot can be due either to destruction of the neurohypophysis or to a change in its functional state ( 30 ). This is essential to bear in mind in the context of the MRI findings in patients with the different types of diabetes insipidus (see the article by JH Christensen and GL Robertson [Chapter 3] in this issue). Biochemistry Vasopressin is synthesized as part of a larger precursor protein encoded by the arginine vasopressin ( AVP ) gene ( Figure 2-2 ). In people, the AVP gene is located quite close to the tip of the short arm of chromosome 20 (20p13) ( 31 ). The gene is small and covers 2500 base pairs. It comprises 3 small exons. The gene encoding the oxytocin hormone, the OXT gene, is located very close to the AVP gene with an intergenic distance of base pairs (see Figure 2-2 ). The 2 genes share the same structure, and they have very similar nucleotide sequences, indicating that they are closely related (eg, they are more than 93% identical in exon 2). However, their organization is unusual in that they are transcribed from opposite DNA strands, implying a tail-to-tail orientation (see Figure 2-2 ). It is generally believed that the 2 genes have evolved separately from a common ancestral gene via gene duplication and inversion ( 32 ). As many as 97% of the magnocellular neurons in the SON are found to abundantly and selectively express either the OXT or the AVP gene, indicating that the cell-specific regulation of the expression of the 2 genes is highly selective. It has recently been found that the cell-specific expression of the OXT and AVP genes is achieved through very limited genomic OXT > < AVP 216 bp 432 bp 178 bp 288 bp 3,053,000 3,064,000 3,065,000 FIG 2-2. Genomic organization of the AVP and OXT genes. The size and location of the genomic regions through which cell-specific expression of the genes is achieved are indicated. Physiology of Vasopressin Secretion and Thirst 31

6 regions comprising, respectively, as little as 216 base pairs upstream and 432 base pairs downstream of the OXT gene and 288 base pairs upstream and 178 base pairs downstream of the AVP gene (see Figure 2-2 ) ( 33 ). Specific regulatory elements within these regions as well as their associated transcription factors remain to be identified. The vasopressin precursor protein encoded by the AVP gene is composed of 4 domains: 1) a signal peptide, 2) the vasopressin moiety, 3) a larger protein domain designated neurophysin 2, and 4) an N-glycosylated moiety named copeptin (please see Chapter 3, figure 3-3 in this issue). The vasopressin moiety is connected to the neurophysin 2 domain by a 3-amino acid residue linker (glycine-lysine-arginine), and the neurophysin 2 domain is connected to copeptin by a 1 amino acid residue linker (arginine). Posttranslational processing of the vasopressin precursor protein results in the generation of 3 secreted protein chains, namely the vasopressin hormone, the neurophysin 2 protein, and copeptin. As noted previously in Chapter 1 (Figure 1-2), the primary amino acid sequences of the vasopressin and oxytocin moieties comprise 9 residues that are identical except at positions 3 and 8. The neurophysin 2 domain, comprising 93 amino acid residues, is remarkably well conserved among all vertebrate and invertebrate species, especially with regard to the central region encoded by exon 2 ( 34 ). The C-terminal domain of the vasopressin precursor protein, copeptin, comprises a sequence of 39 amino acid residues that is glycosylated. This domain, which is absent in the oxytocin precursor protein, is also well conserved and is cleaved by proteolytic processing from the neurophysin 2 moiety. Its physiologic relevance, if any, remains unknown, but it has been suggested that copeptin assists refolding of misfolded vasopressin precursor protein through its interaction with the calnexin-calreticulin protein quality control system in the endoplasmic reticulum (ER) ( 35 ). As copeptin appears to be coreleased with vasopressin into the circulation, it has been investigated as a surrogate marker for vasopressin. However, the reliability of this approach for evaluation of vasopressin secretion has not yet been established, because it is not yet clear if copeptin is distributed and cleared from plasma and extra cellular fluid the same as vasopressin. As with other proteins destined for secretion, the vasopressin precursor protein enters the ER as soon as it is formed owing to the presence of the 19 amino acid residue signal peptide (please see Chapter 3, figure 3-3 in this issue). In the ER lumen, the signal peptide is cleaved by signal peptidase, an enzyme that is located at the luminal surface of the ER membrane. As an important step to allow further intracellular trafficking of the vasopressin precursor protein from the ER, it encounters components of the ER 32 Translational Endocrinology & Metabolism: Posterior Pituitary Update

7 protein quality control system comprising various chaperones and folding enzymes ( 36 ). Chaperones assist the newly synthesized protein to achieve its proper 3-dimensional structure by facilitating folding, preventing untimely intrachain and interchain interactions, and hindering premature intracellular trafficking of misfolded or unassembled further intracellular trafficking As an important step to allow proteins ( 37, 38 ). ER chaperones redirect of the vasopressin precursor misfolded proteins to the cytosolic proteasome, where they are degraded. The spe- encounters components of the protein from the ER, it cific set of chaperones interacting with the ER protein quality control vasopressin prohormone has not been system. established. In the case of the vasopressin precursor protein, the ordered formation of 8 disulphide bridges 1 within the vasopressin moiety and 7 within the neurophysin 2 domain seems to govern the initial folding of the vasopressin moiety and the stepwise folding of the neurophysin 2 domain into a metastable state ( 39 ). Subsequent insertion of the cyclic N-terminal domain of the vasopressin moiety into the binding pocket of neurophysin 2 ( ) stabilizes the vasopressin precursor protein in its correct conformation and enhances self-association into dimers ( 43 ). Efficient binding of the vasopressin moiety to the neurophysin 2 binding pocket is highly dependent on the presence of the α -amino group of the cysteine residue at position 1 and the phenyl ring of the tyrosine residue at position 2. When proper 3-dimensional conformation and dimerization have been achieved, the vasopressin precursor protein moves from the ER to the Golgi apparatus, where it is sorted into the regulated secretory pathway, probably by selective aggregation and packaging into large densecore secretory vesicles in the trans-golgi network of the cell ( 44 ). It is likely that the aggregation occurs spontaneously owing to high local concentrations and inherent physiochemical properties of the vasopressin precursor protein. The final transformation of the vasopressin precursor protein into bioactive vasopressin is initiated in the ER or the Golgi apparatus by enzymatic cleavage between neurophysin 2 and copeptin. This cleavage takes place primarily in the large dense-core vesicles during their maturation and transportation from the cell body to the axon terminals. It involves an enzymatic cascade including: 1) cleavage at the dibasic sequence (lysinearginine) between the vasopressin moiety and neurophysin 2 by a calciumdependent endopeptidase (prohormone convertase), 2) removal of the C-terminal basic amino acid residues that remain after endopeptidase cleavage by a carboxypeptidase B-like enzyme, and 3) conversion of the remaining Physiology of Vasopressin Secretion and Thirst 33

8 C-terminal glycine residue into a C-terminal α -amide by the combined actions of a peptidyl-glycine monooxygenase and an amidating peptidylhydroxyglycine lyase ( 45 ). The resulting biologically active vasopressin hormone probably retains reversible noncovalent interactions with neurophysin 2 while contained within the secretory vesicles, but once secreted into the circulation, they dissociate ( 46 ). The rate of vasopressin synthesis appears to be coupled loosely to the rate of its secretion. In rats, an osmotic stimulus that increases vasopressin secretion also increases the hypothalamic content of vasopressin mrna ( 47 ). This increase coincides with the decrease in vasopressin immunoactivity in the posterior pituitary but precedes the decrease in the hypothalamus. When the stimulus is removed, vasopressin mrna remains elevated even after vasopressin in the pituitary and hypothalamus return to normal. Consequently, pituitary stores of the hormone continue to rise to almost twice the normal basal level. The reason for the prolonged elevation in vasopressin synthesis in this circumstance has not been determined, but it may simply reflect the time required to inactivate the mrna. The rate of vasopressin The increase in vasopressin synthesis is synthesis appears to be also specific to the neurons that respond to coupled loosely to the rate of its the stimulus ( 48 ). Thus, osmotic stimulation increases vasopressin mrna in the vasopressin synthesis is also secretion. The increase in magnocellular neurons that project to the specific to the neurons that posterior pituitary but not in the parvocellular neurons that project to the chiasmatic respond to the stimulus. nucleus. Conversely, adrenalectomy increases vasopressin mrna in parvocellular neurons that project from the PVN to the median eminence and portal veins but not in the magnocellular neurons that project to the posterior pituitary ( 49 ). However, the increase in mrna is not limited to the mrna of vasopressin. In magnocellular neurons, for example, osmotic stimulation also increases the mrna of prodynorphin ( 50 ) and apelin ( 51 ), 2 other peptides that coexist and may be cosecreted with vasopressin. The link between vasopressin synthesis and secretion also seems to work in the reverse (ie, reduced secretion reduces synthesis of the hormone) ( 52 ). The mechanism that links vasopressin synthesis to secretion is unknown. Several factors appear to be involved in regulating vasopressin gene expression ( 53 ), and it is possible that increasing secretion also activates synthesis in neurons that ordinarily do not produce vasopressin ( 54 ). Some of the transcription factors and other basic cellular mechanisms involved in stimulus-synthesis coupling have been elucidated in rats ( 55, 56 ). 34 Translational Endocrinology & Metabolism: Posterior Pituitary Update

9 Secretion Under normal conditions, the most important determinant of vasopressin secretion is the effective osmotic pressure of plasma and extracellular fluid ( ). This influence is mediated by a specialized group of cells, known as osmoreceptors, which are located in the anterior hypothalamus separate from the neurohypophysis ( 63 ). The critical areas appear to be the median preoptic nucleus (MnPO), the subfornical organ (SFO), and the organum vasculosum of the lamina terminalis (OVLT) ( 64, 65 ). The SFO or OVLT may contain the osmoreceptors themselves, since this area lacks a blood-brain barrier, allowing direct contact with the systemic circulation. At the very least, they are critical links specific to the osmoregulatory system, because ablating them abolishes the osmotic stimulation of vasopressin without altering the response to nonosmotic stimuli ( 64 ). As discussed more fully in Chapter 3 of this issue by JH Christensen and GL Robertson, a similar selective loss of osmoregulation has also been found in patients with adipsic hypernatremia due to lesions in the hypothalamus ( 66 ). The mechanism by which the osmoreceptors detect and respond to very small changes in the tonicity of plasma and extracellular fluid is not completely clear. Verney first proposed that they react to small changes in cell volume induced by osmotically driven shifts in water into or out of the cell ( 57 ). This theory is fully consistent with the findings of subsequent studies comparing the effects of different solutes (see below). Recently, it has been suggested that the osmotically driven changes in osmoreceptor volume are converted into electrical signals via mechanosensitive cation channels ( 67 ). The osmoregulation of vasopressin works like a threshold or set-point control system ( 58, 68, 69 ). At plasma osmolarities below a certain level, secretion virtually ceases, and plasma vasopressin falls to less than 1 pg/ml. Above this threshold, plasma vasopressin rises steeply in a close relationship to the increase in plasma osmolarity ( Figure 2-3A ). The response is so sensitive that a rise in plasma osmolarity of only 1% (2.8 mosmols/l) typically increases plasma vasopressin enough to raise urine osmolarity from <100 to nearly 500 mosmols/l ( Figure 2-3B ). The magnitude of the response does not depend on the associated change in blood volume, since it is similar during dehydration or hypertonic saline infusion ( 70 ). Only the thresholds differ, being slightly lower during dehydration owing to the effect of the volume depletion. However, both the set and sensitivity of the osmoregulatory system differ from person to person ( ). These individual differences are relatively large, reproducible on repeat testing ( 74, 75 ) and appear to be genetically determined ( 74, 76 ). On average, they do not differ appreciably Physiology of Vasopressin Secretion and Thirst 35

10 FIG 2-3. Schematic representation of osmoregulatory system. Panel A indicates the level of plasma vasopressin (closed squares) and thirst (closed diamonds) as a function of the concurrent plasma osmolarity in a typical healthy adult. Panel B indicates the level of urine osmolarity (closed squares) and daily urine volume (closed triangles) as function of the concurrent plasma vasopressin. However, individual differences in each of these relationships is relatively large. Among healthy adults, the osmotic threshold for vasopressin secretion varies from 275 to 295 mosmoles/l and the slope or sensitivity of the response can vary almost 10-fold from 0.25 to 1.8 pg/ml per mosmols/l (76). between blacks and whites ( 77 ) or men and women, but they do change during pregnancy and the luteal phase of the menstrual cycle (see below). The osmoreceptors are not equally sensitive to all solutes ( 57, 62, 78, 79 ). In healthy dogs and people, increases in plasma osmolarity produced by infusions of hypertonic sucrose, mannitol, or sodium and its anions stimulate thirst and vasopressin secretion by similar amounts, but infusions of hypertonic urea or glucose have little or a negative effect. These observations are consistent with the theory of how the osmoreceptors work, since the differences between the solutes correlates negatively with their ability to enter cells. Those, like sucrose, mannitol, and sodium, which enter cells slowly or not at all, create an osmotic gradient that dehydrates the osmoreceptors, triggering a change in their electrical activity. Urea and glucose, on the other hand, have little or no stimulatory effect, because they enter cells readily. This means that vasopressin and thirst are controlled not by sodium receptors but by true osmoreceptors, which are differentially sensitive to the extracellular concentration of solutes that affect intracellular volume. The weak stimulatory effect of urea 36 Translational Endocrinology & Metabolism: Posterior Pituitary Update

11 also indicates that the osmoreceptors are located outside the blood-brain barrier, since, unlike the membranes of most cells, this barrier is relatively impermeable to urea ( 78, 79 ). Were the osmoreceptors behind the bloodbrain barrier, they would be stimulated by a rise in plasma urea, since this solute does not cross the barrier. As a consequence, it creates a hydro-osmotic gradient that raises the sodium concentration in the extracellular fluid of brain ( 79 ). The same conclusion can be drawn from the effect of insulinopenia, which sensitizes the osmoreceptor to stimulation by hyperglycemia, indicating that the osmoreceptors also require insulin for rapid uptake of glucose ( 80 ). Thus, the solute specificity of the osmoreceptors is fully consistent with the anatomic studies, which suggests they are located in or near the OVLT, an area of the hypothalamus located outside of the blood brain-barrier ( 64 ). Hemodynamic Acute hypovolemia or hypotension also stimulates vasopressin release ( 68, 81, 82 ). The increases are proportional to the fall in blood volume or pressure, but the relationships are exponential ( 58 60, ). Thus, plasma vasopressin does not rise significantly until blood volume or blood pressure falls by more than 10% to 15% ( 70, 86, 87 ). The stimulatory effect of hypovolemia does not depend on a decrease in blood pressure ( 88 ). However, the volume control mechanism seems to adapt to sustained stimulation, because the vasopressin response diminishes with time, even though the pituitary store of the hormone and the response to osmotic or hypotensive stimuli are unchanged ( 89 ). Acute increases in blood volume or pressure appear to be slightly inhibitory ( ). However, the set of control systems may also adapt to sustained increases in pressure, because osmoregulation appears normal in patients with essential hypertension ( 93 ). Changes in blood volume or pressure large enough to affect vasopressin secretion do not override the effects of plasma osmolarity/sodium ( 94 ). Instead, they appear to act by changing the set or sensitivity of the osmoregulatory system ( 59, 70, 85, ). Thus, vasopressin secretion is still sensitive to osmotic influences, but the threshold for the response is reduced or raised depending on whether blood volume is decreased (eg, by water deprivation) or increased (eg, by hypertonic saline infusion). However, in the presence of moderate hypovolemia, osmotic suppression of vasopressin does not decrease urine osmolarity or increase water excretion as quickly or completely as normal even when plasma vasopressin is depressed to undetectable levels ( 98 ). Thus, the ability to prevent water Physiology of Vasopressin Secretion and Thirst 37

12 intoxication is significantly impaired. The cause of the impairment is not altogether clear but probably includes a reduction in glomerular filtration and increased proximal tubular readsorption of sodium as well as other changes in renal function. The mechanisms that mediate hemodynamic influences on vasopressin secretion have not been completely defined. However, they appear to involve vagal afferents that project from receptors in the heart and aorta ( 99, 100 ) to synapses in the parabrachial nucleus and nucleus tractus solitarius of the brain stem, thence to higher centers in the caudal ventrolateral medulla and from there to the neurohypophysis. The pathway that mediates hypovolemic stimuli probably has at least 1 opioidergic synapse, because systemic administration of the nonspecific opioid antagonist diprenorphine abolishes the vasopressin response to hypovolemia without altering the response to osmotic or hypotensive stimuli ( 101 ). One such synapse may be in the parabrachial nucleus, since diprenorphine has the same effect when microinjected there ( 102 ). The opioid receptors that mediate the vasopressin response to hypovolemia appear to be of the kappa-2 or kappa-3 subtype, and their stimulatory effects are partially restrained or opposed by simultaneous activation of a distinct inhibitory pathway mediated by kappa-1 or mu-receptor agonists ( 103, 104 ). Galanin may also be a neurotransmitter at 1 or more synapses in this inhibitory pathway ( 105 ). In addition, angiotensin II may mediate some of the effects of hemodynamic stimuli, since, in animals, it has been shown to stimulate thirst and vasopressin release, apparently by acting via components of the SFO and OVLT that are also involved in osmoregulation ( 64 ). Nausea is a very rapid and potent stimulus for vasopressin secretion ( 106, 107 ). The vasopressin response commences with the onset of nausea and is not dependent on vomiting, hypotension, or a rise in osmolarity. Like the other vasopressin stimuli, the magnitude and timing of the response vary enormously from person to person. Plasma vasopressin peaks ranging from 14 to more than 500 pg/ml occur 9 to 45 minutes after administration of an emetic stimulus such as apomorphine. The response may be blunted slightly by water loading, but the levels of plasma vasopressin produced are still more than sufficient to produce maximum antidiuresis that lasts for an hour or more. In a few healthy adults, vasopressin secretion is not stimulated by nausea, or it starts to rise before nausea is reported ( 108 ). The effect on vasopressin also does not depend on the cause of the nausea. In addition to apomorphine, it is produced by motion sickness ( 106 ), digoxin ( 109 ), lithium carbonate, copper sulfate and cholecyhstokinin ( 110 ), meptazinol and pentazocine ( 111 ), chemotherapy ( 112 ), and vasovagal reactions (unpublished data, GL Robertson MD). It probably also occurs 38 Translational Endocrinology & Metabolism: Posterior Pituitary Update

13 in hyperemesis gravidarum ( 113 ). The reported exceptions are bingeing with vomiting that usually is not associated with nausea ( 114 ), meal-induced gastric distension to the point of extreme satiety but not nausea ( 108 ), and, possibly, ipecac ( 115 ), although the latter was a powerful nonosmotic stimulant of vasopressin in a child with adipsic hypernatremia ( 116 ). The nausea and increase in plasma vasopressin produced by apomorphine is completely prevented by pretreatment with antiemetics such as haloperidol or fluphenazine ( 107 ) but not naloxone ( 117 ). Because nausea and acute hypotension are both potent stimuli, and either can be triggered by a vasovagal reaction to the simple act of drawing blood, they are potential confounds in almost any study of vasopressin function. Other influences Early observations that pain or fear induced by electrical shock produced antidiuresis in conscious water-loaded dogs initiated the belief that emotional stress is also a stimulus for release of antidiuretic hormone ( 118 ). Subsequent studies in rats ( 119, 120 ) and people ( 121 ) were consistent with this idea, but other studies in the same species were not ( ). If anything, several of the latter studies suggested that emotional stress or noxious stimuli tended to transiently inhibit vasopressin secretion. The most likely explanation for the discrepancy is that stress per se does not stimulate vasopressin release unless it triggers a vasovagal reaction, which typically includes acute nausea or hypotension and results in massive release of the hormone ( 127 )(unpublished data, GL Robertson MD). Unexplained and often large elevations in plasma vasopressin have also been observed in anesthetized people and dogs during and for several days or hours after surgery, particularly of the gastrointestinal (GI) tract ( 128, 129 ). The increase in dogs during partial gastrectomy was attributed to activation of ascending spinal pathways that transmit pain, because they were attenuated by cervical cordotomy or dorsal rhizotomy but not by truncal or cervical vagotomy. However, the rise of vasopressin cannot be attributed to perception of pain, because it occurred while the animals were anesthetized. Additionally, these ascending spinal pathways could convey emetic stimuli arising from surgical trauma to the stomach. The elevations in plasma vasopressin produced by osmotic stimulation can also be suppressed very rapidly by some unknown nonosmotic, nonhemodynamic mechanism activated by drinking rapidly a large volume of fluid ( ). In people, the fall in vasopressin begins immediately with the onset of drinking, before there is a significant fall in plasma osmolarity Physiology of Vasopressin Secretion and Thirst 39

14 or sodium, and it is virtually complete within 10 to 30 minutes, a remarkably rapid fall considering the modest rate at which the hormone is normally cleared ( 58 ). The fall in vasopressin is not associated with changes in blood volume or pressure, and, at least in sheep and/or dogs, it is similar if normal saline instead of water is drunk or the fluid is rapidly removed from the stomach. However, the fall in vasopressin is less marked if the fluid is given by stomach tube, suggesting that some kind of sensor in the oropharynx may be involved. Thirst By stimulating the ingestion of water, thirst is an indispensable adjunct to vasopressin in regulating the tonicity of body fluids. However, thirst is difficult to define precisely and quantitate experimentally, because it is a subjective sensation; additionally, the word means different things to different people. The usual definition, a conscious desire to drink, can include a feeling of dry mouth. This does not always indicate dehydration, since it can result from other unrelated factors such as intense anxiety or rapid mouth breathing. The only objective indicator currently available is the rate of water intake. It too can be misleading, however, because there are a number of other motives for drinking ( 134 ). The drinking that occurs under basal conditions is usually associated with eating and appears to be motivated more by taste than by true thirst. Fluid intake can also be motivated by a variety of external influences such as health fads promoted by the popular press ( 135 ) or flavoring added to various beverages. Despite these problems, however, it has been possible to clarify somewhat the function of the thirst mechanism by measuring the rate of water intake and/or estimating thirst intensity on a linear analogue scale under different experimentally controlled conditions. Regulation Thirst is also regulated primarily by osmoreceptors located in the anterior hypothalamus ( ). Like those for vasopressin, the osmoreceptors for thirst are very sensitive to increases in the plasma concentration of sodium, mannitol, sucrose, and certain other solutes but are insensitive to increases in plasma urea and glucose ( 62, 78 ). In healthy adults, a rise in plasma osmolarity and sodium of only about 1% above basal levels induces a conscious desire to drink, and this desire increases rapidly at levels above 310 mosmols/l and 155 mmols/l, respectively. However, the slope of the relationship between plasma osmolarity and reports of thirst 40 Translational Endocrinology & Metabolism: Posterior Pituitary Update

15 intensity differ considerably between individuals ( 75, 76 ). As with vasopressin, these individual differences are reproducible and appear to be a function of genetic variance ( 76 ). The osmotic threshold for thirst also varies significantly depending on the method used to determine it. If it is determined as the level of plasma osmolarity at which drinking or the desire to drink begins to increase during hypertonic saline infusion, the threshold for thirst is slightly higher than that for vasopressin secretion ( 73, 76, 140, 141 ). However, if thirst is scored on a linear scale and assigned a value greater than zero under basal conditions, the threshold determined by linear extrapolation of the entire relationship back to zero is lower than that for vasopressin secretion ( 142 ). This result has been used to argue that the osmoreceptors for thirst and vasopressin are functionality if not anatomically the same. However, this concept does not reflect the way the osmoregulatory system actually works, because the relationship of thirst intensity to plasma osmolarity is curvilinear and the low levels reported under basal conditions clearly are not strong enough to motivate an increase in drinking until plasma osmolarity rises 1% to 2% above the basal level. If it were otherwise, the result would be a state of perpetual primary polydipsia and polyuria. The osmoregulation of thirst may also include an inhibitory component because lowering plasma osmolarity and sodium by inhibiting water excretion also suppresses drinking ( 143 ). However, this mechanism is not very effective, since approximately 20% of healthy people continue to drink slightly more than their urinary and insensible loss and eventually develop mild hypoosmolarity and hyponatremia when their ability to excrete water is impaired by exogenous administration of antidiuretic hormone. An acute reduction in body water without an increase in osmotic pressure also stimulates an increase in water intake, at least in rats ( 144 ). Like vasopressin, the increase in drinking is proportional to the magnitude of the hypovolemia, but the relationship is curvilinear. Thus, there is little or no increase in drinking until body fluid falls by more than 10%. The effect of hypovolemia on thirst has not been studied in people. It probably exists, however, since patients with severe isotonic blood loss often report thirst. Like vasopressin, osmotically stimulated thirst can be reduced at least transiently by some unknown nonosmotic, nonhemodynamic mechanism triggered by rapid drinking per se ( 62, 133, 145 ). In people, the decrease in thirst commences with drinking and is virtually complete in 15 to 30 minutes, by which time the initial bout of drinking stops even though plasma osmolarity and sodium remain elevated, and blood volume and pressure are unchanged. The satiation is only temporary, however, because thirst and drinking resume 15 to 30 minutes later, and these bouts of Physiology of Vasopressin Secretion and Thirst 41

16 drinking may continue for an hour or 2 until plasma osmolarity and sodium return to basal levels. The mechanism of the temporary satiation is unknown. It is not mediated by osmoreceptors in the GI tract, because, in dogs, the same decrease in drinking occurs if the fluid ingested is normal saline rather than water. The regions of cortical brain activated or deactivated in healthy people when thirst is stimulated by hyperosmolarity have been investigated by positron emission tomography (PET) scanning and functional MRI ( 146 ). In addition to the anterior hypothalamus, which contains the osmoreceptors themselves, these regions are located in various phylogenetically ancient structures involved in other vegetative functions. They include the anterior and posterior cingulate, the parahippocampal gyrus, insula, inferior frontal gyrus, and cerebellum. Unlike many of the other areas of activation, that in the anterior cingulate disappears in association with the temporary satiation of thirst that occurs immediately after drinking even though plasma osmolarity remains elevated. The relation between this activity and the volume of water drunk initially differs in the young and the elderly ( 147 ), perhaps accounting at least in part for the predisposition of the latter to hypertonic dehydration. However, the changes in cortical activity that occur when plasma osmolarity is restored to normal during successive bouts of drinking have not be investigated, and additional studies are needed to determine which of these areas is/are directly involved in the conscious awareness of thirst and which is/are secondary responses to that awareness or even some other physiologically unrelated effects of the rise in plasma osmolarity. These questions might be partly answered by similar studies in patients with adipsia due to damage to the anterior hypothalamus by tumors and other diseases (please see article by JH Christensen and GL Robertson [Chapter 3] in this issue). Interaction of Vasopressin and Thirst in Osmoregulation of Body Fluids The principal action of vasopressin is to conserve body water by reducing the volume of urine required to excrete solutes such as urea, sodium, potassium, and chloride. This is achieved by promoting the reabsorption of water from diluted tubular filtrate as it passes through collecting tubules of the kidney (please see articles by DG Bichet [Chapter 4] as well as JH Christensen and GL Robertson [Chapter 3] in this issue for a more detailed discussion of the mechanisms). The result is to increase total urinary solute concentration (osmolarity) in direct proportion to the reduction in urine 42 Translational Endocrinology & Metabolism: Posterior Pituitary Update

17 volume (see Figure 2-3B ). The magnitude of this antidiuretic effect varies not only with the plasma vasopressin concentration but also with the solute load and the level of hypertonicity in the renal medulla. The maximum antidi uresis achievable in people on a standard diet approximates a urine osmolarity of 1000 to 1200 mosmols/l and a urine flow of 0.5 to 0.6 ml/min (600 to 800 ml/d). Depending on the individual, this limit is usually achieved at a plasma vasopressin concentration between 2 and 4 pg/ml. Higher levels of vasopressin do not result in greater antidiuresis because of the limitations imposed by the solute load and the level of medullary hypertonicity achievable in the human kidney. Consequently, even under conditions of maximum antidiuresis, there is an obligatory loss of water from the kidneys as well as from skin and lungs ( 148 ), and these losses must be continuously replaced by drinking in order to prevent hypertonic dehydration. This protection is normally afforded by the thirst mechanism. The effect of thirst on fluid intake is quite remarkable. In people, the rate of fluid intake under basal conditions normally averages about 90 ml/h during the day ( Figure 2-4 ), and most if not all of that occurs in discrete bouts of drinking during meals. If the tonicity of body fluids increases, thirst is stimulated and, on average, the rate of ad libitum drinking almost doubles for every 1% rise in plasma osmolarity ( 76 ). Even greater rates of drinking (1500 ml in 30 minutes) occur after a total rise in plasma osmolarity of about 6% ( 133 ). Assuming the water ingested is fully absorbed in 90 minutes and antidiuresis is maximal, drinking at these rates would be expected to restore the tonicity of body fluids to normal in 2 to 4 hours. Thus, the thirst mechanism provides a very effective barrier against hypertonic dehydration provided the individual is conscious and able to obtain an adequate supply of potable water. Anything that impairs the thirst mechanism or otherwise interferes with the ability to drink predisposes to the development of hypernatremia-hypertonicity (please see article by JH Christensen and GL Robertson [Chapter 3] in this issue for a more detailed discussion of hyperosmolar syndromes). The prevention of hypotonicity and hyponatremia, on the other hand, is normally afforded by the capacity to osmotically suppress plasma vasopressin and mount a maximum water diuresis. Under these conditions, the solute concentration or osmolarity of the urine is very low (40-80 mosmols/l ) and the volume or rate of output is very high (from L/d depending on body size and the solute load). The capacity of the kidney to excrete water at such high rates provides a very effective barrier against the development of water intoxication due to excessive Physiology of Vasopressin Secretion and Thirst 43

18 FIG 2-4. Circadian pattern of plasma osmolarity, plasma vasopressin, and water balance in healthy adults. intake. Thus, if renal function and solute excretion rates are normal, the osmotic threshold for vasopressin secretion normally determines the lower limit for the tonicity of body fluids. Conversely, anything that lowers that set point (such as hypovolemia) or interferes with the capacity to osmotically suppress vasopressin secretion (such as syndrome of inappropriate 44 Translational Endocrinology & Metabolism: Posterior Pituitary Update

19 secretion of antidiuretic hormone) predisposes to the development of hypoosmolarity and hyponatremia if fluid intake is excessive. The net effect of the 2 osmoregulatory systems is to clamp the extracellular concentration of sodium and related solutes within a very narrow range about halfway between the osmotic thresholds for thirst and vasopressin secretion ( Figure 2-4 ). At this level, plasma vasopressin is relatively constant around 1 pg/ml, urine osmolarity is about half of maximum, thirst is minimal, and urine output and fluid intake are relatively low, on average about 2 L and 3 L per day, respectively. At night, fluid intake is normally zero, and urine output decreases owing largely to a significant decrease in urinary solute excretion. Body water, as reflected in body weight, is also relatively constant, although it usually increases about 1 kg during the day due to slight retention of salt and water caused by eating and upright posture. Physiologic Alterations Pregnancy temporarily alters the set of the osmoregulatory system ( 149 ). Plasma osmolarity and sodium decline in parallel about 5 weeks after conception, stabilize at a level about 3% to 4% (10 mosmols/l or 5 mmols/l) below preconception values by 10 weeks, and remain there until delivery ( 150 ). These changes are due to parallel reductions in the osmotic thresholds for thirst and vasopressin secretion ( 151, 152 ). Thus, there is little or no change in plasma vasopressin, urine osmolarity, or urine output during the first or second trimester either under basal conditions, after fluid deprivation, or during hypertonic saline infusion. In the third trimester, the slope or sensitivity of the vasopressin response to osmotic stimulation also may be reduced slightly, possibly as a result of an increase in vasopressin degradation by a vasopressinase made in the placenta (please see article by JH Christensen and GL Robertson [Chapter 3] in this issue, particularly the section on gestational diabetes insipidus). All of these changes return to preconception values by 10 to 12 weeks after delivery. The cause of the resetting has not been established definitively, but is thought to be closely associated with increases in plasma human chorionic gonadotropin (hcg) ( 152 ), which affects osmoregulation similarly in the absence of pregnancy ( 153 ). Other possible causes include relaxin ( 149 ) or high levels of estrogen ( 154 ). Rats undergo similar changes in osmoregulation during pregnancy ( 155 ), even when they have severe neurohypophyseal diabetes insipidus due to a mutation in the AVP gene ( 156 ). In these animals the reduction in plasma osmolarity and sodium appears to be achieved largely, if not solely, by a massive increase in the rate of Physiology of Vasopressin Secretion and Thirst 45

20 fluid intake that results from decreasing the osmotic threshold for thirst. In normal rats, the resetting of the osmoregulatory system induced by pregnancy is not attributable to hypovolemia and is not associated with any change in the vasopressin response to hypovolemic stimuli ( 157 ). The effect of the menstrual cycle on osmoregulation is similar to but smaller than pregnancy. There is little or no change in basal plasma vasopressin throughout the cycle ( 158, 159 ), but plasma osmolarity and sodium decrease about 1% to 2% in the luteal phase due to parallel reductions in the osmotic thresholds for vasopressin secretion and thirst ( 160, 161 ). This downward resetting cannot be accounted for by a reduction in blood volume or pressure, and it also appears to be independent of the concurrent rise in plasma progesterone ( 162 ). However, it could be secondary to a fall in plasma estrogen from the relatively high levels present during the follicular phase ( 154, 163 ). The effect of luteinizing hormone (LH) on osmoregulation has not been investigated, but, given its chemical and biological similarities to hcg, its rise during the luteum could also be responsible for producing the menstrual changes in osmoregulation so similar to those observed during pregnancy. The effect of aging per se on osmoregulation has been studied extensively but is still somewhat uncertain. Compared to subjects 20 to 60 years of age, the sensitivity of the vasopressin response to osmotic stimulation in the healthy elderly is reported to be increased ( ), unchanged ( ), decreased ( 170 ), or elevated but too erratic to define ( 171 ). The effect of hypotension on vasopressin has been studied less but appears to be diminished or absent in some elderly people ( 84 ). The histology of the SON appears unchanged in the elderly ( 172 ). However, the hyperintense MRI signal emitted by the posterior pituitary is diminished, possibly as a consequence of depletion of vasopressin stores due to increased secretion in response to osmotic stimuli ( 173 ). The effect of aging on thirst is similarly uncertain. The response to osmotic stimulation in the elderly is reported to be decreased ( 165, 167 ) or unchanged ( 166, 169 ). The reason for the lack of consistency in these findings is not known, but several factors could be involved. One is that all the studies of aging are crosssectional rather than longitudinal. Thus, differences or the lack thereof between young and old could be due not to age per se but to age-related genetic differences, which markedly influence the functional properties of the osmoregulatory system ( 76 ). Genetic differences might also selectively remove certain segments of the population from the older age group. It is also possible that some of the differences between the healthy old and young are due not to aging per se but to subtle changes in neurological function, which develop at different ages in everyone and are, 46 Translational Endocrinology & Metabolism: Posterior Pituitary Update

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