Planta Med 2008; 74 - PA139
DOI: 10.1055/s-0028-1084137

Calcium-dependent effect of Tricolorin A on intestinal and arterial smooth muscle contractility

R Hernández 1, A Vuelvas 1, A García 1, M Fragoso 2, R Pereda 2, C Ibarra 1, A Rojas 1
  • 1Laboratorio de Investigación Química y Farmacológica de Productos Naturales, Facultad de Química, Universidad Autónoma de Querétaro, Cerro de las Campanas, 76160, Querétaro, México
  • 2Departamento de Farmacia, Facultad de Química, Universidad Nacional Autónoma de México, Coyoacán, 04510, México D. F., México

In this study we report the effect of Tricolorin A, a resin glycoside isolated from the plant Ipomoea tricolor Cav. (Convolvulaceae), on intestinal and arterial smooth muscle contractility. This compound elicited a concentration-dependent stimulation of spontaneous contractions of the guinea pig ileum (EC50=6.99±1.08µg/ml) and a concentration-dependent vasorelaxation of isolated intact rat aorta (EC50=4.63±1.1µg/ml). Both effects were completely abolished in the absence of extracellular Ca2+. Verapamil (1µM), an L-type voltage-dependent Ca2+ channel blocker, significantly inhibited the contractile response produced by Tricolorin A on the ileum. However, this blocker did not affect the vasodilatory action of this compound. Our findings suggest that the contractions induced by Tricolorin A on the ileum are caused mainly by an increase in Ca2+ permeability that occurs through L-type voltage-dependent Ca2+ channels found in the cell membrane of the smooth muscle. On the other hand, our results indicate that the influx of Ca2+ through L-type voltage-dependent Ca2+ channels does not participate prominently in the vasorelaxant effect elicited by Tricolorin A. Vascular relaxation induced by Tricolorin A was endothelium-dependent and significantly decreased in the presence of nitric oxide synthase (NOS) and soluble guanylate cyclase inhibitors, and a NO scavenger. These results suggest that the vasodilatation produced by Tricolorin A is mainly due to activation of the NO/cGMP pathway, which results from an increased influx of extracellular Ca2+ into the endothelial cells.