Relationship of urotensin I induced vasodilatory action in rat thoracic aorta to Ca2+ regulation.

Abstract

The relaxant effects of the synthetic fish neuropeptide urotensin I were examined in helical strips of rat aorta. In K+-depolarized aorta strips, urotensin I and verapamil competitively inhibited Ca2+-induced contractions. Urotensin I relaxed, in a concentration-dependent manner, the contraction produced by the Ca2+ ionophore A23187, whereas verapamil had no effect on this contraction, even at a concentration of 10(-5) M. In the absence and presence of extracellular Ca2+, urotensin I inhibited both components of the contractions elicited by norepinephrine or urotensin II, another fish neuropeptide. Verapamil reduced only the norepinephrine or urotensin II induced contraction in the presence of extracellular Ca2+, with little or no change in the contraction in Ca2+-free buffer. The urotensin I induced relaxation response in aortic strips contracted by 40 mM KCl was enhanced by pretreatment with papaverine or forskolin. Pretreatment with dibutyryl cAMP did not significantly alter the action of urotensin I. The presence or absence of endothelial cells did not change the response to urotensin I. These results suggest that urotensin I antagonizes the action and (or) mobilization of extracellular and intracellular Ca2+.