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There are reports of the presence of vasodilatory alkaloids in Heimia salicifolia extracts. The action mechanisms of the potential antihypertensive effect of such alkaloids have not however, been elucidated. The objective of the present study was to corroborate the antihypertensive and vasorelaxant activities of the isolated alkaloids from H. salicifolia, and to characterize their vasorelaxant actions. A chloroform extract (HSCE) was obtained from H. salicifolia. The alkaloids were separated by thin layer chromatography, extracted from silica gel, and evaluated using spectroscopy. The alkaloid with the most potent vasorelaxant activity was identified as lythrine. The antihypertensive effect of the HSCE was corroborated on normotensive rats and on animals with Nω-nitro-L-arginine-methyl ester (L-NAME) induced hypertension. The action mechanisms of the HSCE and lythrine were studied on isolated and perfused rat mesenteric vascular bed (MVB) preparations. HSCE administration produced a concentration-dependent relaxation, but in preparations without vascular endothelium, the relaxant response to HSCE was significantly diminished. In MVB preparations with intact vascular endothelium, pre-contracted with phenylephrine or L-NAME, perfusion with lythrine produced concentration-dependent relaxation; a similar effect was produced by acetylcholine. Wortmannin (phosphatidylinositol 3-kinase inhibitor) and methylene blue (guanylate cyclase inhibitor) decreased the relaxant effect of lythrine. These data suggest that the vascular relaxation induced by alkaloids isolated from H. salicifolia is dependent on the activation of the nitric oxide/guanylate cyclase pathway.   Key words: Heimia salicifolia, lythrine alkaloid, hypertension, Nω-nitro-L-arginine-methyl ester (L-NAME), mesenteric vascular bed.

Evaluation of antihypertensive and vasorelaxant effects of Heimia salicifolia (family: Lythraceae)