Abstract
The hypotensive activity of a series of calcium entry blockers and various other vasodilators was quantified in pentobarbitone-anesthetized rats. Hypotensive activity was correlated linearly with the potency of these vasoactive agents to depress α 2-adrenoceptor-induced pressor responses in pithed rats. However, vasodilation as such also influenced α 2-adrenoceptor-mediated vasoconstrictor processes. For this reason, the depressive action of the vasodilating compounds on α 2-adrenoceptor-induced pressor effects was also determined during vasopressin infusion, which counteracted the vasodilation induced by the vasoactive compounds. It was found that the hypotensive activity exerted by the calcium entry blockers was directly related with their inhibitory activity to depress α 2-pressor responses. This relationship was not observed for the other vasodilators. The results provide further evidence for the hypothesis that vasodilatation induced by calcium entry blockers is caused by the selective impairment of that part of the vascular tone which is maintained by vascular postjunctional α 2-adrenoceptors.
Published Version
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