Role of 5-HT2 receptors in serotonin-induced contractions of nonvascular smooth muscle.
Vascular receptors responsible for serotonin-induced contractions are of the 5-HT2 subtype (site in brain cortical membranes that is preferentially radiolabeled by [3H]spiperone) whereas serotonin receptors mediating contraction in nonvascular smooth muscle have not been extensively studied. The present in vitro studies using the 5-HT2 receptor antagonists ketanserin, LY53857 and 1-(1-naphthyl)piperazine show that serotonin-induced contractions in the rat uterus and guinea-pig trachea are also mediated by interaction with 5-HT2 receptors. Prazosin, but not the serotonin receptor antagonists, blocked serotonin-induced contractions in the rat vas deferens, indicating that alpha adrenergic and not 5-HT1 or 5-HT2 receptors mediate the contractile response to serotonin in this tissue. Because selective 5-HT2 receptor antagonists did not block contractions to serotonin in the rat fundus or guinea-pig ileum, receptors in these gastrointestinal tissues are clearly not 5-HT2. However, contractions to serotonin in the fundus but not in the ileum were blocked by certain antagonists [metergoline and 1-(1-naphthyl)piperazine] demonstrating that the receptors involved in serotonin-induced contractions in the fundus are different from the ileum. Other differences between the fundus and ileum in serotonin-induced contractions include: 1) the potency of serotonin is greater in the fundus than in the ileum; and 2) the primary action of serotonin in the fundus is activation of a postsynaptic receptor on the smooth muscle whereas, in the ileum, serotonin exerts an indirect neuronal action to effect acetylcholine release.(ABSTRACT TRUNCATED AT 250 WORDS)[1]References
- Role of 5-HT2 receptors in serotonin-induced contractions of nonvascular smooth muscle. Cohen, M.L., Schenck, K.W., Colbert, W., Wittenauer, L. J. Pharmacol. Exp. Ther. (1985) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
