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Cimetropium: characterization of antimuscarinic and spasmolytic properties.

Cimetropium displaced 3H-NMS binding from membranes derived from gastrointestinal smooth muscle. The affinity of cimetropium for intestinal muscarinic receptors was in the range 70-100 nM. The competitive antagonism of cimetropium was demonstrated in guinea-pig ileum and taenia coli stimulated by bethanechol. Comparing pA2 values, cimetropium (8.19 and 7.91, resp.) was 0.3 times as potent as atropine (8.52 and 8.41, resp.). Cimetropium displayed strong inhibitory effects towards BaCl2 and 5-hydroxytryptamine induced contractions of the guinea-pig ileum. The compound was devoid of antihistaminic or Ca++ channel blocking activity. A binding study performed in vivo confirmed the ability of i.v. cimetropium to displace 3H-N-methylscopolamine binding from muscarinic receptors in peripheral organs. In addition, when injected into ileal loops, cimetropium displaced 3H-NMS binding solely from the surrounding tissue of the loop, indicating a topical effect of the compound.

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[Experiments on the mechanism of action of vascular spasmolytics. 4. Effect of nitroprusside sodium, nitroglycerin, prenylamine and verapamil on the calcium uptake of microsomes of the smooth bascular muscles].

Nitroprusside-sodium, nitroglycerol, and verapamil had no effect on the calcium uptake by microsomes from the carotid artery of cattle. Prenylamine reduced the passive binding and the active uptake and released already bound calcium. The basal Mg-dependendent ATPase and Ca-stimulatable Mg-ATPase were inhibited by prenylamine.

Animals↗