Abstract
Cimetidine produced a dose-dependent and reversible inhibition of contractions of the nictitating membrane elicited through stimulation of the preganglionic nerve supplying the superior cervical ganglion in the anaesthetized cat. Postganglionic nerve stimulation resulted in only a slight and variable inhibition of the contractions. Both hexamethonium and cimetidine also produced a dose-dependent and reversible fall in arterial blood pressure. The ganglion blocking activity of cimetidine was much weaker than that of hexamethonium; the ED50 ratio (cimetidine:hexamethonium) calculated from the cumulative log dose-response curves for the two drugs was 64. The possible mechanism(s) of ganglion blockade produced by cimetidine is discussed including a possible action at nicotinic receptors, either directly or indirectly (via its anticholinesterase activity), and ion channel blockade. The clinical implications of cimetidine-induced ganglionic blockade are also discussed, especially with respect to sexual impotence associated with the use of cimetidine.
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More From: Clinical and experimental pharmacology & physiology
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