Nicotine-sensitive cholinergic receptors (n-cholinergic receptors) are mainly localized on the postsynaptic membranes in the synapses of skeletal muscles, autonomic nerve nodes (ganglia), adrenal medulla and carotid sinus zones (evolutionarily both of the latter formations are ganglia), some interneuronal contacts.
n-anticholinergics have the ability to screen receptors and prevent their excitation by acetylcholine. Thus, the transmission of impulses from the corresponding nerves to the striated muscle, adrenal gland, carotid sinuses, from neuron to neuron from preganglionic to postganglionic autonomic fibers can be blocked.
Under the action of ganglion blockers, autonomic nerve nodes become insensitive not only to endogenous acetylcholine, but also to various exogenous cholinergic stimuli (nicotine, lobelin, cytisine, etc.). Blocked sympathetic and parasympathetic nodes, but for different drugs in different sequences and with different strengths.
By interrupting the conduction of nerve impulses in the ganglia, ganglion blockers change the functions of organs supplied with autonomic innervation. At the same time, blood pressure decreases, the supply of vasoconstrictor impulses to the blood vessels decreases and the peripheral vascular bed, primarily arterioles, decreases, the secretion and peristalsis of the gastrointestinal tract decreases. Initially, ganglion blockers (hexamethonium benzenesulfonate, azamethonium bromide, etc.) were relatively widely used to treat hypertension, gastric ulcer and duodenal ulcer, and other diseases. However, due to the side effects caused by these drugs and the creation of new more effective drugs, ganglion blockers are currently of limited use. Sometimes they are used to relieve hypertensive crises and in the complex therapy of peptic ulcer disease.
Below is a list of n-anticholinergics (ganglion blockers):
- Azamethonium bromide