Drugs Acting on Autonomic Ganglia: Blockers

Ganglionic blockers impede impulse transmission at the autonomic ganglia of the sympathetic and parasympathetic systems.

They can act by various mechanisms. For instance, they can induce persistent depolarization of the postsynaptic neuron or block the release of the neurotransmitter  acetylcholine to prevent neurotransmission.

Some agents act as competitive blockers by binding to the nicotinic receptors, preventing acetylcholine interaction with the receptor. Alternatively, they can function as noncompetitive blockers, obstructing the ion channel essential for neurotransmission.

Most blockers, being ionized, have limited permeability across the membrane.

These blockers are used clinically to manage hypertensive emergencies, aid smoking cessation, and serve as tools in experimental pharmacology.

Blockade of the sympathetic ganglia causes arterial vasodilation, thus reducing blood pressure and potentially causing postural hypotension.

Following hypotension, ganglionic blockers can induce tachycardia and reduce cardiac output.

Conversely, blockade of the parasympathetic ganglia can cause abdominal discomfort, nausea, a dry mouth, syncope, urinary retention, and cycloplegia.