Abstract
Summary
Bradykinin was shown to potentiate the contraction of rabbit aortic strips to 5-HT, NE, and KCl. Forty-two percent of the strips tested responded to bradykinin alone. Butylated hydroxyanisole antagonized the direct contractile effect of bradykinin, but did not attenuate bradykinin-potentiated responses of strips to 5-HT, NE, or KCl. SKF-525A did not affect bradykinin contraction, but did significantly decrease the potentiated response resulting from the interaction of bradykinin with 5-HT, NE, or KCl. It was concluded that bradykinin potentiation of arterial smooth muscle contraction was not mediated through an interaction with adrenergic or serotonergic receptors, but rather through a nonspecific effect at the cell membrane of smooth muscle. It was proposed that bradykinin-induced contraction was mediated through specific bradykinin receptors not present in all the rabbit aortae.
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