Effects of Higenamine on the Contractility of Aorta and Taenia Coli in Guinea-piqs

Abstract

Higenamine isolated from Aconiti tuber is known to have positive inotropic action through the adrenergic ~-receptors. However, the effects of higenamine on the vascular smooth muscle and taenia coli have not yet been elucidated. The actions of higenamine were investigated on the activated aortic strips of guinea-pigs and rabbits by norepinephrine, high K-Tyrode's solution and electrical field stimulation, and also on the spontaneous contractions of guinea-pig taenia coli. Electrical activities and mechanical contractions were simultaneously recorded using the conventional suction-electrode method and single sucrose gap technique. All experiments were performed in tris-buffered Tyrode's solution which was aerated with 100% O2 and kept at 35°C. Higenamine suppressed dose-dependently the norepinephrine-induced contraction. Propranolol potently antagonized the inhibitory effects of higenamine on rabbit aorta, while less potently on guinea-pig aorta. Higenamine seemed to suppress profoundly the component of intracellular Ca2+ mobilization in the contraction curve of norepinephrine in guinea-pig aorta. Higenamine did not seem to suppress the component of Ca2 + influx through the potential-sensitive Ca2 + channel in K-contracture of guinea-pig aorta. Higenamine suppressed both passive resting tension and active tension (phasic contraction) driven by electrical field stimulation (A.C. 60 Hz, 5-7 V/cm, duration 10 sec, interval 3 min) in guinea-pig aorta. Propranolol also rapidly suppressed both passive resting and active tensions. Higenamine dose-dependently suppressed the frequency and amplitude of spontaneous contraction, resulting in complete abolishment of it above 10-6 M concentration in guinea-pig taenia coli. Propranolol almost completely antagonized its effect. Higenamine reduced dose-dependently both burst frequency and spike frequency, and depolarized membrane potential in guinea-pig taenia coli. Propranolol almost completely blocked its effect. In conclusion the inhibitory action of higenamine to the norepinephrine-induced contraction might be produced by the depression of intracellular Ca2+ mobilization and Ca2+-influx through ~-adrenoceptors in guinea-pig aorta. The Ca2+-influx through the potential-sensitive Ca2+ channel might not be suppressed by higenamine in guinea-pig aorta. The inhibitory effects of higenamine on the spontaneous contractions of guineapig taenia coli result from the decrease of burst frequency and spike frequency through the ~-adrenoceptors.