Abstract
The α2‐adrenoceptor agonists TL99 (2‐(NN‐dimethyl)amino‐6,7‐dihydroxy‐1,2,3,4‐tetrahydronaphthalene) and UK14304 (5‐bromo‐6‐[2‐imidazoline‐2‐yl‐aminol]‐quinoxaline), in concentrations that are less than 1% of those producing vasoconstriction, enhance vasoconstrictor responses to noradrenaline and phenylephrine in isolated perfused preparations of the rat tail artery. The enhancing effect was abolished when Ca2+ was absent and by the calcium channel blocking drug diltiazem. α2‐Adrenoceptor agonists had no effect on the component of the responses to noradrenaline and phenylephrine that is attributable to mobilization of intracellular Ca2+, but enhanced the component attributable to influx of extracellular Ca2+. These results suggest that the enhancing effect of α2‐adrenoceptor agonists on responses of the rat tail artery to α1‐adrenoceptor agonists involves an increase in Ca2+‐influx into smooth muscle cells through Ca2+ channels that are opened when α2‐adrenoceptors are activated.

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