Vasorelaxant effect of Hyptis fruticosa Salzm. ex Benth., Lamiaceae, dichloromethane extract on rat mesenteric artery

Vasorelaxant effect of Hyptis fruticosa Salzm. ex Benth., Lamiaceae, dichloromethane extract on rat mesenteric artery

Vasorelaxant effect of Hyptis fruticosa dichloromethane extract (HFDE) on isolated rings of rat mesenteric artery was evaluated in this study. In intact rings, HFDE (0.1-3000 µg/mL) induced concentration-dependent vasorelaxations (Emax = 119±14%; n = 6) of phenylephrine tonus that were not modified after endothelium removal (Emax = 116±6%; n = 6), after KCl 20 mM (Emax = 135±9%; n = 6) or in rings pre-contracted with KCl 80 mM (Emax = 125±4%; n = 6). In endothelium denuded rings, HFDE (300 or 1000 µg/mL) inhibited contractions induced by CaCl2 (maximal inhibition = 25±7% and 95±1%; respectively). Furthermore, HFDE promoted an additional vasorelaxation (15±3%; n = 7) after maximal response of 10 µM nifedipine (78±3%; n = 7). In conclusion, HFDE induces vasorelaxant effect through an endothelium-independent pathway, which appears to be due in major part to inhibition of the Ca2+ influx through voltage-operated Ca2+ channels.

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Bibliographic Details
Main Authors: Moreira,Ítalo J. A., Moreno,Maria P. N., Fernandes,Maria F. G., Fernandes,João B., Moreira,Flávia V., Antoniolli,Ângelo R., Santos,Márcio R.V.
Format: Digital revista
Language:English
Published: Sociedade Brasileira de Farmacognosia 2010
Online Access:http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-695X2010000500018
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Summary:Vasorelaxant effect of Hyptis fruticosa dichloromethane extract (HFDE) on isolated rings of rat mesenteric artery was evaluated in this study. In intact rings, HFDE (0.1-3000 µg/mL) induced concentration-dependent vasorelaxations (Emax = 119±14%; n = 6) of phenylephrine tonus that were not modified after endothelium removal (Emax = 116±6%; n = 6), after KCl 20 mM (Emax = 135±9%; n = 6) or in rings pre-contracted with KCl 80 mM (Emax = 125±4%; n = 6). In endothelium denuded rings, HFDE (300 or 1000 µg/mL) inhibited contractions induced by CaCl2 (maximal inhibition = 25±7% and 95±1%; respectively). Furthermore, HFDE promoted an additional vasorelaxation (15±3%; n = 7) after maximal response of 10 µM nifedipine (78±3%; n = 7). In conclusion, HFDE induces vasorelaxant effect through an endothelium-independent pathway, which appears to be due in major part to inhibition of the Ca2+ influx through voltage-operated Ca2+ channels.

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