| Abstract |
Endothelium-derived hyperpolarizing factors (EDHFs) are the main vasodilatory mediators of resistance arteries which are important in regulating blood pressure. EDHFs have been suggested to compensate for impaired nitric oxide (NO) release in patients with essential hypertension. This study aimed to determine the antihypertensive effect of aqueous extract of Moringa oleifera leaves (MOE) and its effect on EDHF-mediated vasorelaxation in hypertensive rats induced by Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME). Male Wistar rats were administrated with L-NAME (50 mg/kg/day) in drinking water for 3 weeks. Acute hypotensive activity of MOE was tested in anesthetized rats by means of intravenous injection of the extract, and the changes in arterial pressure were measured via femoral artery catheterization. The results showed that MOE (0.1-3 mg/kg) caused a dose-dependent reduction in mean arterial blood pressure (7.13±0.47-29.76±1.86%) with no significant change in heart rate. The vasorelaxant activity of MOE was investigated in resistance arteries using perfused isolated mesenteric arterial beds. The injection of MOE (0.001-0.3 mg in 0.1 ml injection volume) into the perfusate caused a concentration-dependent relaxation with a maximum relaxation of 75.57±1.76% achieved at 0.3 mg which was abolished by endothelium denudation (15.36±1.00%, max. relaxation). The inhibition of NO, PGI2 and H2S productions did not affect the MOE induced endothelium-dependent relaxation (84.76±3.35%, max. relaxation). Interestingly, this persisting relaxation was significantly inhibited by calcium-activated potassium channel blocker (5 mM tetraethylammonium), myoendothelial gap junction inhibitor (10 µM 18α-glycyrrhetinic acid), and high potassium medium (45 mM KCl) with a maximum relaxation of 68.28±1.83, 32.78±1.07, and only 17.90±1.64%, respectively. These findings demonstrate that the endothelium-dependent vasorelaxation in response to MOE may be mediated via EDHF release. Thus, we conclude that MOE has antihypertensive effect possibly by inducing of EDHF mediated vasorelaxation. |
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