Anisodamine inhibits acetylcholine-induced endothelium-dependent relaxation of canine femoral artery.

The effects of anisodamine on acetylcholine-induced endothelium-dependent relaxation were studied in organ chambers and under bioassay conditions. In organ chamber experiments, both acetylcholine and bradykinin induced an endothelium-dependent relaxation of norepinephrine-contracted canine femoral arteries in a concentration-dependent manner; the relaxation induced by acetylcholine, but not that by bradykinin, was inhibited by anisodamine or atropine in a concentration-dependent manner. In bioassay experiments, a denuded ring of left circumflex coronary artery was superfused with perfusate passed through segment of femoral artery with endothelium or a direct superfusion line. Acetylcholine induced the release of relaxing factor(s) from the segment with endothelium causing a relaxation of bioassay ring and the relaxation was eliminated by anisodamine infused into the perfusion line above, but not below, the perfused segment. The results suggest that anisodamine, like atropine, is able to inhibit acetylcholine-induced endothelium-dependent relaxation by blocking endothelial muscarinic receptors which activate the release of endothelium-derived relaxing factor(s).