Abstract

In this study, we examine whether Clitoria ternatea Linn. (CT) can prevent Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced cardiac and vascular dysfunction in rats. Male Sprague Dawley rats were given L-NAME (40 mg/kg, drinking water) and orally administered with CT extract (300 mg/kg/day) or lisinopril (2.5 mg/kg/day) for 5 weeks. The main phytochemical components of the CT extract were found to be flavonoids. The CT extract alleviated the high blood pressure in rats receiving L-NAME. Decreased vasorelaxation responses to acetylcholine and enhanced contractile responses to sympathetic nerve stimulation in aortic rings and mesenteric vascular beds of L-NAME treated rats were ameliorated by CT extract supplementation. Left ventricular hypertrophy and dysfunction were developed in L-NAME rats, which were partially prevented by CT extract treatment. The CT extract alleviated upregulated endothelial nitric oxide synthase expression, decreased plasma nitrate/nitrite levels, and increased oxidative stress in L-NAME rats. It suppressed high levels of serum angiotensin-converting enzyme activity, plasma angiotensin II, and cardiac angiotensin II type 1 receptor, NADPH oxidases 2, nuclear factor-kappa B, and tumor necrosis factor-alpha expression. The CT extract, therefore, partially prevented L-NAME-induced hypertension and cardiovascular alterations in rats. These effects might be related to a reduction in the oxidative stress and renin–angiotensin system activation due to L-NAME in rats.

Highlights

  • Since nitric oxide (NO) was discovered more than 40 years ago, it has been wellestablished as playing a crucial physiological role in blood pressure control [1]

  • We found that the main phytochemical components of Clitoria ternatea Linn. (CT) extract are flavonoids

  • The present study showed an alleviation of oxidative damage in CT extract-treated rats mediated by reduced vascular O2 − production and MDA levels, resulting in increased NO bioavailability, as well as increased endothelial nitric oxide synthase (eNOS) protein expression, in renin–angiotensin system (RAS) activation might be one of the possible mechanisms increasing blood pressure and oxidative stress in L-NAME rats

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Summary

Introduction

Since nitric oxide (NO) was discovered more than 40 years ago, it has been wellestablished as playing a crucial physiological role in blood pressure control [1]. In animal models of hypertension, the blockade of NO synthesis using nitric oxide synthase inhibitors to induce cardiovascular alterations has been well-accepted [3,4]. Chronic inhibition of NO production by Nω-nitro-L-arginine methyl ester (L-NAME) produces high blood pressure, cardiovascular hypertrophy, and dysfunction in rats. These deleterious effects of L-NAME are associated with NO depletion, renin–angiotensin system (RAS) activation, and reactive oxygen species (ROS). Modulation of the RAS has been suggested to participate in the development of hypertension in L-NAME-treated rats, as increased angiotensin-converting

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