Threshold Concentrations of Endothelin‐1: The Effects on Contractions Induced by 5‐Hydroxytryptamine in Isolated Rat Cerebral and Mesenteric Arteries *

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Abstract
This study compares the effects of threshold concentrations of endothelin‐1 in isolated rat basilar arteries with those in mesenteric arterial branches and investigates the mechanisms of inhibitory and potentiating endothelin‐1‐effects. In basilar arteries, endothelin‐1 reduces the contractions induced by 5‐hydroxytryptamine (5‐HT), by the thromboxane A2agonist U46619, and by vasopressin. The inhibitory effect of endothelin‐1 on the contraction induced by 5‐HT is abolished by deendothelialization, by the endothelin ETBreceptor antagonist RES 701–1, by indomethacin, or by glibenclamide. In mesenteric arteries, endothelin‐1 potentiates the contractile effects of 5‐HT, U46619, and vasopressin. The potentiation of the contractile effect induced by 5‐HT is only somewhat modified by deendothelialization, but abolished by the thromboxane A2receptor antagonists GR32191 and ridogrel. U46619 potentiates the 5‐HT‐effect in mesenteric arteries. Thus, though the contractile endothelin ETAreceptors were not blocked, threshold concentrations of endothelin‐1 inhibited contractile effects in the rat basilar artery via activation of endothelial ETBreceptors. Prostaglandins and ATP‐sensitive K+channels are involved in this inhibitory action. In contrast, endothelin‐1 potentiates contractile actions in mesenteric arteries via the release of endogeneous thromboxane A2from non‐endothelial cells. The study points out the completely different role of the endothelium in combined effects of endothelin‐1 between cerebral and mesenteric arteries.

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