Effect of Moringa oleifera leaf extract on blood pressure and vascular reactivity to adrenergic stimulation in L-NAME hypertensive rats

P. Tangsucharit¹, D. Aekthammarat¹, P. Pakdeechote², P. Pannangpetch¹. ¹Pharmacology, Khon Kaen University, Khon Kaen, Thailand, ²Physiology, Khon Kaen University, Khon Kaen, Thailand.

Introduction: Sympathetic overactivity resulting in increased total peripheral resistance plays a major role in pathogenesis of hypertension¹. Moringa oleifera (MOE) (local name: Marum) is a tropical plant distributed in tropical/subtropical including Thailand. The leaf of Moringa oleifera is used in Thai folk medicine for the treatment of many ailments including cardiac and circulatory problems². The present study aims to investigate the preventive effect of aqueous leaf extract of MOE on hemodynamic status and adrenergic reactivity in N^ω-nitro-L-arginine-methylester (L-NAME) induced hypertensive rats.

Methods: Male Wistar rats (n=7/each group) were administered daily with L-NAME (50 mg/kg/day) in drinking water for three weeks and concurrent treatment with MOE (30 or 60 mg/kg, p.o.) or captopril (5 mg/kg/day, p.o.). At the end of experiment, blood pressure and heart rate (HR) were measured under pentobarbital sodium (60 mg/kg, i.p.) anesthesia. Contractile responses to perivascular nerve stimulation (PNS; 2-16 Hz) and exogenous phenylephrine (Phe; 0.01-1.0 mmol) were tested in isolated mesenteric vascular bed³. Data were expressed as mean ± S.E.M. Statistical analysis was tested by one-way analysis of variance (ANOVA) and followed by Student Newman-Keul's test.

Results: Rats treated with L-NAME had higher BP and HR than the value in control rats. Concurrent treatment with MOE or captopril (5 mg/kg/day) prevented these alterations (Table 1, p<0.05). The hemodynamic disturbances were associated with augmented mesenteric reactivity to adrenergic stimulation including PNS and the selective α₁-adrenoceptor agonist in L-NAME rats. Daily MOE-treatment at both low and high doses significantly reduced the reactivity to PNS to the normal levels (Fig.2A, p<0.05). Moreover, oral administration of MOE at doses of 30 and 60 mg/kg resulted in dose-dependent recovery of contractile responses to Phe in L-NAME rats (Fig.2B, p<0.05).

Conclusion: MOE prevents L-NAME induced hypertension in rats, which might involve the suppression of adrenergic hyperactivity. The current results could suggest that MOE might be useful as a dietary supplement against hypertension associated with sympathoexcitation.

References:

1. Koyama T et al.(2010). Hypertens Res 33(5): 485-91.

2. Randriamboavonjy JI et al. (2016). Am J Hypertens 29(7): 873-81.

3. Tangsucharit P et al. (2012). Am J Physiol Regul Integr Comp Physiol 303(11): R1147-56.

Table 1 Effect of MOE on blood pressure and heart rate in L-NAME hypertensive rats