The objective of this study was to examine effects of activation of endothelin (ET) B receptors on tone of the basilar artery in vivo. By using a cranial window in anesthetized rats, we examined the effects of IRL 1620, a selective ET(B) receptor agonist, on diameter of the basilar artery. Under control conditions, diameter of the basilar artery was 214 ± 6 μm (mean ± S.E.). Topical application of IRL 1620 (10-6 mol/l) for 4 min dilated the basilar artery by 30 ± 4%. Marked desensitization of vasodilator responses was observed in response to a second application of IRL 1620, but not acetylcholine, which indicates a homologous nature of desensitization. REA/001, an ET(A)/ET(B) receptor antagonist, abolished IRL 1620-induced dilatation of the basilar artery. BQ 123, a selective ET(A) receptor antagonist, inhibited constriction in response to ET-1, but did not affect dilator responses of the basilar artery to IRL 1620. Both N(G)-nitro-L- arginine methyl ester and N(G)-nitro-L-arginine, inhibitors of nitric oxide synthase, produced marked inhibition of dilator responses of the basilar artery to IRL 1620 without inhibiting vasodilator responses to sodium nitroprusside. Indomethacin did not inhibit vasodilatation in response to IRL 1620. These findings suggest that activation of ET(B) receptors produces dilatation of the basilar artery in vivo. Dilator responses of the basilar artery to activation of ET(B) receptors are dependent on production of nitric oxide.
|ジャーナル||Journal of Pharmacology and Experimental Therapeutics|
|出版ステータス||出版済み - 1995|
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