Postganglionic blockers

The basis for the antihypertensive activity of the ganglionic blockers lies in their ability to block transmission through autonomic ganglia (Fig. 20.2C). This action, which results in a decrease in the number of impulses passing down the postganglionic sympathetic (and parasympathetic) nerves, decreases vascular tone, cardiac output, and blood pressure. These drugs prevent the interaction of acetylcholine (the transmitter of the preganglionic autonomic nerves) with the nicotinic receptors on postsynaptic neuronal membranes of both the sympathetic and parasympathetic nervous systems. 

Ganglion blockers competitively block nicotinic cholinoceptors on postganglionic neurons in both sympathetic and parasympathetic ganglia. In addition, these drugs may directly block the nicotinic acetylcholine channel, in the same fashion as neuromuscular nicotinic blockers (see Figure 27-6). 

Oral 250, 500 mg tablets Parenteral 50 mg/mL for injection Postganglionic Sympathetic Nerve Terminal Blockers Guanadrel (Hylorel)... 

Postganglionic neuron blocker Drug that blocks transmission by an action in the presynaptic postganglionic nerve terminal... 

E. Adrenoceptor Blockers Alpha -selective agents (eg, prazosin) and beta-blockers (eg, propranolol) are effective antihypertensive drugs. Alpha-blockers reduce vascular resistance and venous return. The nonselective alpha-blockers (phentolamine, phenoxybenzamine) are of no value in chronic hypertension because of excessive compensatory responses, especially tachycardia. Alpha,-selective adrenoceptor blockers are relatively free of the severe adverse effects of the nonselective alpha-blockers and postganglionic nerve terminal sympathoplegic agents. 

Which of the following is a postganglionic nerve terminal blocker that has insignificant CNS... 

Postganglionic sympathetic neuron blocker enters nerve ending via uptake-] and effects reversed by TCAs, cocaine. Tox severe orthostatic hypotension, sexual dysfunction. 

It is, however, interesting to observe that a good number of sympathomimetics in fact do not really mimic the actions of noradrenaline or adrenaline at the effector receptor. They merely induce the release of noradrenaline from the sympathetic postganglionic adrenergic nerves. Such sympathomimetics which exert their action indirectly are comparatively less effective in patients treated with noradrenaline depleting drugs, for instance, the rauwolfia alkaloids, or other adrenergic neuron blockers. 

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