In the previous paper, we reported of rats treated chronically with ethanol; that side chain oxidation of hexobarbital, N-demethylation of aminopyrine and p-hydroxylation
1. Using the cannula insertion method, muscarinic receptor subtypes were analysed in isolated, perfused canine lingual arteries preconstricted with phenylephrine. 2. Both acetylcholine and McN-A-343 induced a profound vasodilation in a dose-related manner. Acetylcholine-induced dilations were approximately 1000-times more potent than McN-A-343-induced dilation. 3. Acetylcholine-induced dilations were abolished after removal of the endothelium by intraluminal treatment with 1 mg saponin. 4. Acetylcholine-induced dilations were markedly inhibited by an M1/M3 receptor antagonist, 4-DAMP. Moreover, they were slightly, but significantly, inhibited by an M1 antagonist, pirenzepine, but never influenced by an M2 antagonist, AF-DX 116. Mc-N-A-343-induced vasodilations were inhibited by both 4-DAMP or pirenzepine. 5. These results suggest that there are abundant functional M3 and a few M1 receptors in the canine lingual artery that mediate vasodilation and that this vasodilation is dependent on the presence of an intact endothelium.
The stainless cannula inserting method was used to investigate the effects of alpha-adrenoreceptor agonists (phenylephrine, alpha 1-agonist and xylazine alpha 2-agonist) and calcium chloride on isolated and perfused dog mesenteric arteries with and without saponin treatment. By intraluminal administration, phenylephrine and calcium chloride caused vasoconstriction in a dose-related manner whilst xylazine was without significant effect. After intraluminal treatment with 3 mg of saponin, the endothelia of the arteries were completely removed as confirmed by pathological examinations. Phenylephrine- and xylazine-induced responses were not influenced by saponin treatment whereas calcium chloride-induced constriction was significantly enhanced.
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