Blood Pressure Regulation. Slides 9-12 Mean Arterial Pressure (MAP) = 1/3 systolic pressure + 2/3 diastolic pressure

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1 Sheet physiology(18) Sunday 24-November Blood Pressure Regulation Slides 9-12 Mean Arterial Pressure (MAP) = 1/3 systolic pressure + 2/3 diastolic pressure MAP= Diastolic Pressure+1/3 Pulse Pressure CO=MAP/TPR MAP=CO * TPR So if you want to change pressure MAP,you change either CO or TPR or both. Changing CO by changing Heart Rate (HR), or Stroke volume (SV) or both. How to change TPR? By vasoconstriction or vasodilation,especially arteriols, because they account for 50% of TPR, they are major resistant vessels. Autonomic Nervous System Sympathetic nervous system is important in control of circulation. Parasympathetic nervous system is important in regulating heart function Sympatheticnerve fibers innervate all vessels except capillaries and precapillary sphincters and some metarterioles. Innervation of small arteries and arterioles allow sympathetic nerves to increase vascular resistance. Large veins and the heart are also sympathetically innervated. Parasympathetic nervous system is mainly important in control of heart rate via the vagus nerve.

2 Slides Short term regulation of blood pressure 1-high pressure baroreceptors 2-low pressure baroreceptors 3-chemoreceptors High pressure baroreceptors (also called pressoreceptors) are located in aorta and carotid artery (refer to slide 14) The Vasomotor Center (VMC) The VMC transmits impulses downward through the cord to almost all blood vessels. VMC is located bilaterally in the reticular substance of the medulla and the lower third of the pons. The VMC is composed of a vasoconstrictor area, vasodilator area, and sensory area. Reflex is initiated by stretch receptors called baroreceptors or pressoreceptors located in the walls of the large systemic arteries. A rise in pressure stretches baroreceptors and causes them to transmit signals to the VMC and feedback signals are sent via the automonic nervous system to the circulation to reduce arterial pressure (AP) back to normal. Baroreceptors have basal rate of firing, working best around normal MAP=100mmHg, and that is why we call them buffering system for blood pressure, while buffering system for ph work best at normal pka. Baroreceptors since they are neural they work very fast, account for short term regulation of blood pressure milliseconds. They correct blood pressure to normal, they do not increase or decrease BP above or below normal.

3 They are not important in long term control of arterial pressure because the baroreceptors adapt. So if there is increase in blood pressure for prolonged period of time, baroreceptors adapt that condition and change there basal rate, for example, if BP is 120mmHg for prolonged period of time baroreseptor adapt that condtion, and now if BP decrease to 100 baroreceptors sense that change and send signals to vasomotor centers(vmc) in order to decrease BP to 120 (basal value). Normally basal value is around 100mmHg. Experiment Cutting baroreceptors in the blood vessels of an animal, now blood vessels become denervated, when that animal stand or lying down blood pressure vary significantly. So baroreceptors are important in short term regulation of BP. Function of the Baroreceptors Maintains relatively constant pressure despite changes in body posture. Response of the Baroreceptors to Arterial Pressure Carotid sinus baroreceptors respond to pressures between 60 and 180 mmhg. Baroreceptors respond to changes in arterial pressure.

4 Baroreceptors reflex is most sensitive at a pressure of 100mmHg. As pressure increases the number of impulses from carotid sinus increases which results in: 1) inhibition of the vasoconstrictor 2) activation of the vagal center (refer to silde 18,19 for baroreceptor mechanism to restore BP) Slide 21 Intrinsic control frank-starling law Extrinsic control inotropic effect Refere to slide 22 for Effect of Parasympathetic and Sympathetic Nervous Systems on Factors that Influence the Mean Arterial Pressure (the Dr. read the slide) Slides low pressure baroreceptors Located at Rt. Atrium, Rt. Ventricle and Pulmonary artery Sensitive to changes in Volume Two mechanisms for low pressure baroreceptors: 1-atrium hypothalamic reflex 2-atrium kidney reflex First: atrium hypothalamic reflex An increase in volume increase in venous return increase in cardiac output increase in MAP and vice versa

5 This work through atrial-hypothalamic reflex through stimulating Anti Diuretic Hormone (ADH) -Vasopressin-in case of low BP or inhibiting ADH in case of high BP i.e this will affect the volume and so the BP through its effect on urine output and also on TPR since ADH (Vasopressin) is strong vasoconstrictor. Low BP stimulate ADH High BP inhibit ADH Second: atrium kidney reflex Low pressure baroreceptors work also through affecting the Glomerular Filtration Rate (GFR) by causing Afferent arteriolar dilation in case of high BP due to high volume or Vasoconstriction in case of low BP due to low volume Affecting the GFR means affecting the urine volume In case of increased BP increased pressure in Rt atrium vasodilation of afferent arteriol increase blood flow to kidney increase GFR increase urine output decrease volume correct BP to normal slide chemoreceptors Chemoreceptors are chemosensitive cells sensitive to oxygen lack, CO2 excess, or H ion excess. Chemoreceptors are located in carotid bodies near the carotid bifurcation and on the arch of the aorta. Activation of chemosensitive receptors results in excitation of the vasomotor center(vmc). Chemoreceptors are stimulated when blood pressure falls below 80mmHg Remember baroreceptors respond to increase or decrease of BP above or below 100mmHg.

6 Now we will start with blood pressure regulation(2) Slide 2 Intermediate term control hormones Long term control renal body fluid system Slide 3 factors affecting TPR Blood viscosity(plasma proteins, RBCs) Arterial radius (extrinsic control, intrinsic contol) Extrinsic contol ADH, Angiotensin II, sympathetic activity norepinephrine, epinephrine. Intrinsit contor myogenic activity of smooth muscle cells in the vessel wall, heart contractility, local metabolities Refer to slide 4 and 5 (the Dr. read them) Slides 6-7 CNS Ischemic response is systemic response due to cerebral ischemia, when MAP falls below 60mmHg. Reduced cerebral blood flow causes CO 2 buildup which stimulates vasomotor center(vmc) thereby increasing arterial pressure. CNS Ischemic response is one of the most powerful activators of the sympathetic vasoconstrictor system. CNS Ischemic response is not activated until pressure falls below 60mmHg, greatest activation occurs at pressures of 15-20mmHg. Cushing reaction is a special type of CNS ischemic response. Prolonged CNS ischemia has a depressant effect on the vasomotor center. Slides 8-10 Atrial and Pulmonary Artery Reflexes Low pressure receptors in atria and pulmonary arteries minimize arterial pressure changes in response to changes in blood volume.(the Dr. read the slides)

7 Slide 11 Renal Body Fluid System for Long Term Arterial Pressure Control Plays a dominant role in long term pressure control. As extracellular fluid volume increases arterial pressure increases. The increase in arterial pressure causes the kidneys to lose Na and water which returns extracellular fluid volume to normal. Experiment Giving an individual iv infusion of fluid, increases blood volume, increases venous return, increases EDV, increases CO, increases BP, Increased BP will activate Renal Body Fluid System which will increase urine output thus lowering volume returning BP to normal. Normally input = output Slide 12 Pressure Natriuresis and Diuresis The effect of pressure to increase water excretion is called pressure diuresis. The effect of pressure to increase Na excretion is called pressure natriuresis Note: below 60mmHg no urine output Slide Graphical Analysis of Renal Body Fluid Mechanism The major determinants of long-term arterial pressure control. -Based on renal function curve -Salt and water intake line Equilibrium point is where intake and output curves intersect. Renal body fluid feedback system has an infinite gain Gain =correction/error

8 Baroreceptors has very gain. Baroreceptors do not bring pressure to its accurate normal pressure it has error. Example(1) baroreceptors short term regulation Normally MAP=100mmHg, suddenly it rises to 120mmHg, then baroreceptors are activated, lowering BP TO 105mmHg. Correction= =15 Error= =5 Gain=correction/error = 15/5=3 Example(2) renal body fluid system Renal body fluid system correct BP to So correction= = Error= = (very small) Gain=correction/error= / =very large number ~usually we say infinite. Note in slide 13 Angiotensin converting enzyme inhibitors (ACEI) shift the curve to the left Slides14-17 Failure of Total Peripheral Resistance to Elevate Long-term Arterial Pressure Changes in TPR does not affect long-term arterial pressure level. One must alter the renal function curve in order to have long-term changes in arterial pressure. Changing renal vascular resistance does lead to long-term changes in arterial pressure. Sodium is a Major Determinant of ECFV As Na+intake is increased; Na+stimulates drinking, increased Na+concentration stimulates thirst and ADH secretion. Changes in Na+intake leads to changes in extracellular fluid volume (ECFV). ECFV is determined by the balance of Na+intake and output.

9 Slides Intermediate / Long term Regulation of BP 1. Epinephrine Adrenal medulla system works as intermediate term needs10 min. to work causes vasoconstriction 2. ADH (vasopressin) system needs 30 min to work causes vasoconstriction 3. Renin-Angiotensin-Aldosterone system needs 1 hour to be effective Angiotensinogen (14 a.a peptide) converted into Angiotensin I (10 a.a peptide) by Renin that come from afferent arteriolar cell, the angiotensin I is converted into angiotensin II (8 a.a peptide) by Angiotensin converting enzyme mainly in the lungs. Angiotensin II (AII) is very potent vasoconstrictor. AII also stimulates aldosterone synthesis and secretion from the adrenal coretx (Zona glomerulosa), aldosterone increases Na+ reabsorption from the renal nephrone and so water. AII is also a positive inotropic agent. Note vasodilators are for acute hypertension(emergency condition) but it is not used for chronic hypertention,long term regulation of BP, why? Becease using vasodilators for long term, although TPR decreases but at the same time CO increases so MAP does not change. MAP=CO*TPR Example: an individual has a car accident and has hemorrhage which decrease blood volume and thus decrease pressure. First baroreceptors are stimulated in order to increase BP (first 10minutes) Second epinephrine-adrenal medulla system (after 10minutes) 3 rd ADH system (after 30 minutes) 4 th Rennin-angiotensin-aldosterone system (after 1 hour) Note decreased BP inhibit anti natriuretic peptide (ANP) Done by Atef Al-Lami

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