Vasorelaxant effects of 1-nitro-2-phenylethene in rat isolated aortic rings.

Loeste Arruda-Barbosa, Karilane Maria Silvino Rodrigues, Francisco das Chagas Vasconcelos Souza-Neto, Gloria Pinto Duarte, Rosivaldo S Borges, Pedro Jorge Caldas Magalhães, Saad Lahlou

Index: Vascul. Pharmacol. 63(2) , 55-62, (2014)

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Abstract

Previously, we showed that nitro-2-phenylethane is a vasorelaxant constituent of the essential oil of Aniba canelilla. Here, we investigated the mechanisms underlying the vascular effects of 1-nitro-2-phenylethene (NPe), a structural analog of 1-nitro-2-phenylethane obtained synthetically, in rat isolated thoracic aortic preparations. At 0.1-100 μg/mL, NPe similarly relaxed endothelium-intact or endothelium-denuded aortic preparations pre-contracted with 60mM KCl or with phenylephrine (PHE, 1 μM). Vasorelaxant effects of NPe against PHE-induced contractions remained unaffected following blockade of potassium channels by TEA, and inhibition of either nitric oxide synthase by l-NAME, cyclooxygenase by indomethacin or guanylate cyclase by ODQ. In preparations maintained under Ca(2+)-free conditions, NPe significantly reduced the contractions induced (i) by PHE, but not those evoked by caffeine, (ii) by CaCl2 in either PHE (in the presence of 1 μM verapamil)- or KCl-stimulated preparations, (iii) by extracellular Ca(2+) restoration in thapsigargin-treated aortic preparations, and (iv) by the activator of protein kinase C phorbol-12,13-dibutyrate or the inhibitor of protein tyrosine phosphatase sodium orthovanadate. It is concluded that NPe induced an endothelium-independent vasorelaxation with potency greater than its structural analog 1-nitro-2-phenylethane. Such action appears to occur intracellularly probably through inhibition of contractile events that are clearly independent of Ca(2+) influx from the extracellular milieu.Copyright © 2014 Elsevier Inc. All rights reserved.