(PP VIII) Dr. Samir Matloob
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1 DRUGS ACTING ON THE CHOLINERGIC SYSTEM AND THE NEUROMUSCULAR BLOCKING DRUGS I (DIRECT ACTING CHOLINOMIMETIC AGONISTS) (PP VIII) Dr. Samir Matloob Dept. of Pharmacology Baghdad College of Medicine
2 Drugs Acting On The Cholinergic System And The Neuromuscular Blocking Drugs Classify neuromuscular blocking drugs, describe their mechanisms of action, report their clinical applications, state their adverse effects and interpret their interactions. Objectives and intended learning outcomes: The student should be able to List the locations and types of acetylcholine receptors in the major organ systems. Describe the steps in the synthesis, storage,release and fate of acetylcholine. Classify cholinomimetics and describe their actions, uses and adverse effects. Classify different muscarinic antagonists and describe their actions, uses, adverse effects and contraindications. Describe the effects of nicotine and the ganglion-blocking drugs.
3 Drugs acting on the cholinergic system Direct acting cholinomimetic agonists Objectives and intended learning outcomes: The student should be able to List the locations and types of acetylcholine receptors in the major organ systems. Describe the steps in the synthesis, storage, release and fate of acetylcholine. Classify cholinomimetics and describe their actions, uses and adverse effects.
4 The autonomic nervous system (ANS) has two parts: the sympathetic and the parasympathetic Now consider the following about the ANS: 1-Spinal roots of origin: The parasympathetic fibers originate from the 3 rd, 7 th, 9 th & 10 th cranial n. and from S2-S4 segments of the spinal cord, while the sympathetic preganglionic fibers originate in the thoracic T1-T12 & Lumber L1-L5. 2-Location of the ganglia: In the PANS ( parasympathetic ANS ) the ganglia are close to the innervated organ (ie.the preganglionic fiber is long and the postganglionic fiber is short ) the opposite is true for SANS (sympathetic ANS) because most of the sympathetic ganglia are located in the paravertebral chains that lie along the spinal column
5 3- Innervations of organs: a- the motor efferent portion of the PANS is one of the motor pathways for transmission of information from CNS to the effector tissues (smooth m., cardiac m., exocrine glands). b- uninnervated receptors: some receptors that respond to autonomic transmitters and drugs receive no innervations e.g. some muscarinic receptors on the endothelium of blood vessels & some presynaptic receptors.
6 4- Neurotransmitters: a. At the preganglionic synapse of the SANS & PANS the mediator is Ach. b. At the postganglionic synapse the neurotransmitter in the PANS is Ach while in the SANS it is norepinephrine (noradrenalin) with exception of the thermoregulatory sweat gland (Acrine sweat gland) & some blood vessels to skeletal m. where the mediator is Ach.
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10 Synthesis: Ach is synthesized from acetyl co A and choline by the enzyme choline acetyl transferase. the rate limiting step is probably the transport of choline into the nerve terminal. This step is blocked by hemicholinium. Storage: Ach is actively transported into the vesicles for storage. This process is inhibited by vesamicole Release: This occurs when an action potential propagated by the action of the voltage sensitive Na channels arrives at the nerve ending. The release of Ach requires entry of Ca ions (through Ca voltage gated channels which become opened) and triggering interaction between several proteins associated with the vesicle and nerve ending membrane (synaptobrevin, snap and others)
11 The interaction results in the fusion of the vesicular membrane and nerve ending membrane and release of their contents into the synaptic space. Botuloinum toxin blocks the release of Ach. While (by contrast) black widow spider venom causes the release of all Ach stored in the vesicles. Binding to receptor: Released Ach diffuses cross the synaptic space & bind either to postsynaptic receptor on the target cells or to presynaptic receptor in the membrane of the neuron that released the Ach.
12 Termination of the action of Ach: It is terminated in the synapse by metabolism of Ach to acetate & choline by the enzyme acetylcholine esterase. Inhibition of those enzymes is important in the therapeutic effect of many drugs. Recycling of choline: Choline is captured by Na coupled uptake system that transports the molecules back into the neuron where it is acetylated and stored until released by a subsequent action potential (AP).
13 Cholinergic receptors (cholinoceptors): These are subdivided into muscarinic & nicotinic receptors. Muscarinic receptors (MRs): These receptors are G coupled protein receptors. Respond to muscarine as well as Ach. The effects of activation of these receptors resemble those of postganglionic PANS stimulation. Muuscarinic receptors are located primarily on autonomic effector cells including: heart, vascular endothelium, smooth m., presynaptic nerve terminal and exocrine glands. Types: M1,M2,M3,M4,M5 but the first three types are the most important.
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15 Nicotinic receptors (NRs): These are ion cannel receptors. Respond to nicotine (another Ach mimic) but not to muscarine. There are two major subtypes of nicotinic receptors: (Nn) located in the ganglia and (Nm) located at the neuromuscular end plate of skeletal m. Nicotinic receptors are also found in the adrenal medulla and CNS
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17 R Location Post R. Mechanism M1 Nerve ending Increase IP3, DAG cascade M2 Heart, some nerve endings Decrease CAMP, activate K channels M3 Effector cells: smooth m.,glands,endoth. Increase IP3,DAG cascade Nn ANS ganglia Na/K depolarizing current (evokes AP) Nm N-M junction Na/K depolarizing current
18 Mechanisms of Ach signal transduction(post receptor mechanisms) Muscarinic mechanism: Several mechanisms have been defined for muscarinic receptors: 1- The mechanism for M1 & M3 receptors: When M1 & M3 are activated (1) they undergo conformational change & (2) interact with a G protein which in turn (3) activates phospholipase C (a membrane bound enzyme) leading to (4) release of second messengers DAG (DiAcyl Glecerol) and IP3 (inositol 1,4,5,triphosphate). DAG modulates the action of protein kinase C, an enzyme important in secretion while IP3 evokes the release of Ca from intracellular storage sites which results in contraction.
19 of 2- The mechanisms for M2 receptors : a- Couples M2 to adenylyl cyclase through an inhibitory G protein which leads to decrease cyclic AMP production. b- Couples M2 receptor directly to K channel in the heart Muscarinic agonists facilitate the opening of these channels.
20 Nicotinic mechanism: The receptor is located on the channel protein that is selective to Na & K. When the receptor is activated the channel opens and depolarization of the cell occurs (EPSP) as a direct result of the influx of Na. Those receptors are present on the ganglionic cells (of both SANS & PANS) & the neuromuscular junction.
21 Cholinergic drugs: cholinergic drugs are of two types: 1-Direct acting agonists: acts directly on cholinoceptors. 2- indirect acting agonists (anticholinesterase):acts by inhibiting the action of cholinesterase accumulation of Ach in the synaptic space
22 Direct acting cholinomimetic agonists: These drugs mimic the action of Ach by binding directly to cholinoceptors. Those agents are either: 1- Choline esters e.g. Ach, Methacoline, Carbacol and Bethanecol. 2- Naturally occurring alkaloids e.g. Muscarine, pilocorpine and Nicotine. These drugs differ in their spectrum of action to muscarinic or nicotinic stimulation, e.g. pilocarpine & Bethanecol preferentially bind to MRs.,however direct acting drugs (as a group) show little specify in their action
23 Effects of direct acting cholinoceptors agonists (Only the direct effects are indicated, hemostaticresponses to these direct actions may be important) Organ Response CNS Eye Sphincter m. Ciliary m. Heart SA node AV node Atria Ventricles Blood vessels Bronchi complex stimulatory effects e.g. nicotine (elevation of mood) miosis (constriction of the pupil) contraction (accommodation) to near vision heart rate (-ve chronotropy) conduction velocity (-ve chronotrophy), R.P (refractory period) contractile strength (-ve intropy), R.P small in contractile strength dilation via EDRF (endothelium derived relaxation factor) (NO) bronchoconsriction GIT Motility Sphincters Urinary bladder detrusor trigon & sphinctor Skeletal m, Glands relaxation via ENS (enteric nervous system) contraction relaxation (1) activation of N-M end plate (2) contraction of m. secretion of thermoregulatory sweat, lacrimal, bronchial, gastric and intestinal glands
24 NOTES: Vasodilatation and decreased blood pressure is not evoked by PANS discharge... why? -Because it is mediated by the action of uninervated muscarinic receptors found in blood vessels which are stimulated by directly acting muscarinics (muscarinic agonists),normally theses receptors have no function because Ach is never released into the blood in significant quantities, stimulation of these receptors leads to the release of NO (EDRF) which causes the vasodilatation. Decreased blood pressure evokes a baroceptor reflex resulting in a strong sympathetic discharge to the heart, thus the result may be tachycardia rather than bradycardia. Another effect seen with directly acting drugs but not with PANS stimulation is thermoregulatory sweating, this is a sympathetic-cholinergic effect.
25 Clinical uses: We can predict the major clinical application of muscarinics from a consideration of organs and diseases that benefit from an increase in cholinergic activity. Ach: Acetylcholine is quaternary Ammonium ester that is rapidly hydrolysed by acetylcholine esterase & plasma cholinesterase (pseudo cholinesterase); Ach therapeutically is of no importance. Why? Because of: (1) Its multiplicity of actions and (2) Its rapid inactivation by cholinesterase (5-30 sec.).
26 Bethanecol: Structurally, it is related to Ach but it is more resistant to hydrolysis by ChE (cholinesterase) It has strong muscarinic activity but no nicotinic action. It is orally active,its duration of action is 30 min 2 hrs. Its action is mainly on the smooth m. of the GIT and bladder; therefore, it is used to stimulate the bowel and bladder post operatively
27 Carbachol: Has both muscarinic & nicotinic actions It is poor substance for ChE. It causes the release of epinephrine from the adrenal medulla by its nicotinic action. Duration of action is one hour. It is used topically as a miotic agent & to decrease IOP (intraocular pressure).
28 pilocarpine
29 Pilocarpine: It is an alkaloid & is stable to hydrolysis by ChE. It exhibits muscarinic activity. Duration of action is 30m 2 hrs. It is primarily used in ophthalmology & it is the drug of choice in the emergency lowering the IOP both in narrow angle and wide angle glaucoma. Pilocapine is extremely effective in the opening of trabecular meshwork around schlemns canal causing an immediate drop of IOP as a result of increased drainage of aqueous humor. Pilocapine can enter the brain and can cause CNS disturbances.
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32 Toxicity: The signs and symptoms of over dosage are readily predicted from the general pharmacology of Ach Toxicity includes CNS stimulation, miosis, spasm of accommodation, bronchoconstriction, GIT and genitourinary smooth m. activity, secretion activity of (sweat gland, airways and GIT) and vasodilatation. Transient bradychardia followed by reflex tachycardia if the drug is administrated I.V.
33 SUMMARY.Ach is the neurotransmitter at the preganglionic synapse for both the SANS & PANS and also at the postganglionic synapse of the PANS. Cholinergic recptors are of two types. Muscarinic and Nicotinic. Muscarinic R. are found primarily on autonomic effector cells including: heart, vascular endothelium, smooth m., presynaptic nerve terminal and exocrine glands Nicotinic R. are two major subtypes of nicotinic receptors: (Nn) located in the ganglia and (Nm) located at the neuromuscular end plate of skeletal m. Direct acting cholinomimetic agonists mimic the action of Ach by binding directly to cholinoceptors.these agents are either choline esters or natural alkaloids.
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