Effects of alpha-adrenoceptor antagonists on electrical and mechanical responses of the isolated dog mesenteric vein to perivascular nerve stimulation and exogenous noradrenaline

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Abstract
The effects of four different α-adrenoceptor antagonists (prazosin, phentolamine, yohimbine, and nipradilol) on the electrical and mechanical responses of smooth muscle cells of the dog isolated mesenteric vein to perivascular nerve stimulation and exogenous noradrenaline were investigated. Perivascular nerve stimulation generated an excitatory junction potential (e.j.p.), a spike potential and a slow depolarization. The latter component was blocked by yohimbine or phentolamine at doses over 10−7 M, while the former two components were suppressed by 10−6–10−5 M yohimbine, but not by prazosin, nipradilol or phentolamine (up to 10−5 M). Nerve-mediated muscle contractions were suppressed by these α-adrenoceptor antagonists in a concentration-dependent manner, at doses over 10−7 M. The order of potency was yohimbine > nipradilol = phentolamine > prazosin. Exogenously applied noradrenaline (10−6 M) depolarized the smooth muscle membrane and generated slow waves. The slow waves were blocked by all of these α-adrenoceptor antagonists (10−5 M), while the depolarizations were inhibited by yohimbine (>10−7 M) or phentolamine (10−5 M), but not by nipradilol or prazosin (up to 10−5 M). Contrictions produced by exogenously applied noradrenaline (10−6 M) were inhibited by the α-adrenoceptor antagonists; yohimbine or phentolamine (10−6–10−5 M) showed complete inhibition and prazosin or nipradilol (up to 10−5 M) partial inhibition. Contractions produced by high-potassium or current-stimulation were suppressed by high-concentrations (10−6–10−5 M) of these α-adrenoceptor antagonists. These observations indicate that the smooth muscle of the dog mesenteric vein possesses mainly α2-adrenoceptors, and stimulation of these receptors produces membrane depolarization and muscle contraction. High-concentrations of α-adrenoceptor antagonists have inhibitory effects on the muscle contraction by blocking α-adrenoceptors and also by other mechanisms.

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