Abstract
The fish neuropeptide urotensin II (UII, 10 nM) caused a 51% increase in uptake of 45Ca by segments of rat aorta; this increase was abolished by the Ca channel blocking drug nitrendipine (200 nM). 45Ca efflux was unchanged in the presence of UII, but was significantly increased following washout of the peptide; again, this increase was not observed in the presence of nitrendipine. The results provide direct evidence that the nitrendipine-sensitive component of the contractile response of rat aorta to UII involves mobilization of extracellular Ca, with subsequent activation of a Ca-induced, Ca-release process intracellularly. The mechanisms responsible for the nitrendipine-resistant component of the contractile response to UII remain to be established.
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