Endothelium-derived nitric oxide is involved in the hypotensive and vasorelaxant responses induced by the aqueous fraction of the ethanolic extract of the leaves of Albizia inopinata (Harms) G. P. Lewis in rats.

The acute cardiovascular effects of an aqueous fraction of the ethanolic extract of the leaves (AFL) of Albizia inopinata (Harms) G. P. Lewis (Leguminosae) were studied in rats using a combined in vivo and in vitro approach. In conscious, unrestrained rats, AFL (5, 10 and 20 mg/kg(-1) body wt. i.v., randomly) produced a significant and dose-dependent hypotension associated with increases in heart rate and cardiac output, and with a strong reduction in total peripheral resistances. The hypotensive response to AFL (20 mg/kg(-1) body wt.) was attenuated significantly after nitric oxide (NO) synthase blockade (L-NAME, 20 mg/kg(-1) body wt. i.v.). Furthermore, under these conditions, the associated tachycardia was inhibited completely. In isolated rat aortic rings, increasing concentrations of AFL (10, 20, 40 and 80 microg/ml(-1)) were able to antagonize the effects of phenylephrine- (1 microM) and KCl- (80 mM) induced contractions (IC50 value 65 +/- 4 and 54 +/- 6 microg/ml(-1), respectively). The smooth muscle-relaxant activity of AFL was inhibited similarly either removal of the vascular endothelium or by L-NAME (10 and 100 microM), but was not affected significantly by atropine (1 microM) or indomethacin (10 microM). In isolated rat atrial preparations, AFL (30, 100, 300 and 500 microg/ml(-1)) produced concentration-related negative inotropic and chronotropic effects (IC50 value = 274 +/- 53 and 335 +/- 23 microg/ml(-1), respectively). These results suggest that in rats, the hypotensive effect of AFL is due to a peripheral vasodilation, at least partly secondary to the release of NO by the vascular endothelium. The direct cardio-depressant actions of AFL are of little importance in the systemic effects of the extract.