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Evidence-Based Complementary and Alternative Medicine
Volume 2012 (2012), Article ID 472821, 8 pages
Research Article

The ent-15 -Acetoxykaur-16-en-19-oic Acid Relaxes Rat Artery Mesenteric Superior via Endothelium-Dependent and Endothelium-Independent Mechanisms

1Escola de Enfermagem e Farmácia, Universidade Federal de Alagoas, Cidade Universitária, Tabuleiro dos Martins, 57072-970 Maceió, AL, Brazil
2Laboratório de Tecnologia Farmacêutica, Universidade Federal da Paraíba, P.O. Box 5009, 58051-970 João Pessoa, PB, Brazil
3Departamento de Farmácia, CCBS, Universidade Estadual da Paraíba, 58100-000 Campina Grande, PB, Brazil

Received 21 August 2012; Revised 7 November 2012; Accepted 13 November 2012

Academic Editor: Jairo Kenupp Bastos

Copyright © 2012 Êurica Adélia Nogueira Ribeiro et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The objective of the study was to investigate the mechanism of the relaxant activity of the ent-15α-acetoxykaur-16-en-19-oic acid (KA-acetoxy). In rat mesenteric artery rings, KA-acetoxy induced a concentration-dependent relaxation in vessels precontracted with phenylephrine. In the absence of endothelium, the vasorelaxation was significantly shifted to the right without reduction of the maximum effect. Endothelium-dependent relaxation was significantly attenuated by pretreatment with L-NAME, an inhibitor of the NO-synthase (NOS), indomethacin, an inhibitor of the cyclooxygenase, L-NAME + indomethacin, atropine, a nonselective antagonist of the muscarinic receptors, ODQ, selective inhibitor of the guanylyl cyclase enzyme, or hydroxocobalamin, a nitric oxide scavenger. The relaxation was completely reversed in the presence of L-NAME + 1 mM L-arginine or L-arginine, an NO precursor. Diterpene-induced relaxation was not affected by TEA, a nonselective inhibitor of K+ channels. The KA-acetoxy antagonized CaCl2-induced contractions in a concentration-dependent manner and also inhibited an 80 mM KCl-induced contraction. The KA-acetoxy did not interfere with Ca2+ release from intracellular stores. The vasorelaxant induced by KA-acetoxy seems to involve the inhibition of the Ca2+ influx and also, at least in part, by endothelial muscarinic receptors activation, NO and PGI2 release.