Reversible Anticholinestrase :
(Edrophonium , Physostigmine , Neostigmine ... )
It binds reversibly to the active center of AchE preventing hydrolysis of Ach. This leads to accumulation of Ach at cholinergic nerve endings and thus increase its effect.
Irreversible Anticholinestrase :
( Echothiophate , Organophosphate )
It binds covalently via its phosphate group to the serine-OH group at the active site of AchE. This leads to permanent inactivation of AchE and the enzyme has to be re-synthesized.
Anti-muscarinics :
( Atropine , Hyoscine , Ipratrobium ..... )
It competes with Ach at muscarinic receptors and prevents Ach from binding to those sites.
Depolarizing Ganglionic Blockers :
( Nicotine )
It depolarizes nicotinic receptors in autonomic ganglia producing stimulation of post-ganglionic sympathetic and parasympathetic fibers. And in large dose , it produce persistent depolarization of nicotinic receptors leading to its block.
Competitive Ganglionic Blockers :
( Trimetaphan )
It competes with Ach at nicotinic receptors in autonomic ganglia and prevents Ach from binding to those receptors.
Depolarizing Neuromuscular Blockers:
( Succinylcholine )
It depolarizes the plasma membrane of the muscle fiber but they resist degradation by AchE, so providing constant stimulation of the receptors , and this renders the receptors incapable of transmitting further impulses and leads to flaccid paralysis.
Competitive Neuromuscular Blockers :
( Curare , Atracurium .... )
It competes with Ach at neuromuscular junctions and prevents Ach from binding to those receptors.
Indirect acting adrenergic agonists :
( Amphetamine )
It causes release of catecholamines from vesicles in adrenergic neuron and thus leads to elevation of the levels of catecholamines in synaptic spaces.
( Cocaine )
It blocks the Na/K ATPase on the cell membrane of adrenergic neuron. thus , it blocks nor-epinephrine uptake and it accumulates in the synaptic space > enhancement in sympathetic activity.
( Ephedrine )
It induces the release of nor-epinephrine from presynaptic terminals and activate adrenergic receptors on the postsynaptic membrane.
α-Blockers :
( Phenoxybenzamine )
It binds covalently to α1 and α2 receptors and block them irreversibly so that , they have to be re-synthesized by the body.
( Phentolamine , Prazosin .... )
All other α-blockers are selective or non-selective competitive blockers > It competes with catecholamines for α1 ( or α2 ) receptors.
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*** - Non-selective competitive blocker > Phentolamine ************
*** - Selective α1 competitive blocker > Prazosin , Terazosin , Doxazosin ************
*** - Selective α2 competitve blocker > Yohimbine ************
*** - Non-competitive α blocker > Phenoxybenzamine ************
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β-Blockers :
(All β-blockers are competitive antagonists) > It competes with catecholamines for β1 ( or β2 ) receptors.
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*** - Non-selective β-blocker > Propranolol , Timolol , Nadolol ************
*** - Selective β1-blocker > Acebutolol , Atenolol , Metoprolol , Esmolol ************
*** - Partial β Agonist > Pindolol , Acebutolol ************
*** - α and β blocker > Labetalol , Carvedilol ************
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Reserpine :
It blocks Mg/ATP dependent transport of catecholamines from the cytoplasm into storage vesicles in the adrenergic nerves. This causes the ultimate depletion of biogenic amines.
Guanethidine :
It blocks the release of the stored nor-epinephrine from storage vesicles. This leads to gradual depletion of nor-epinephrine in nerve endings.
NEXT PART : MECHANISM OF ACTION FOR ALL DRUGS ACTING ON CNS.
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