Abstract

Nω-nitro-l-arginine methyl ester (L-NAME) is a non-specific nitric oxide (NO) synthase inhibitor, commonly used for the induction of NO-deficient hypertension. The objective of the present study was to investigate the effects of chrysin with flavnoids, on L-NAME-induced hypertensive rats. Methods: An experimental hypertensive animal (180–220 g) model was induced by L-NAME intake on rats. In treatment chrysin was orally administered 25 mg/kg body weight (b.w.). Blood pressure was measured by tail cuff plethysmography system. Cardiac and vascular function was evaluated by Langendorff isolated heart system with Angiotensin II (Ang-II), Hexo oxygenase (HO-1), cyclic guanosine monophosphate (cGMP) concentration in tissues respectively. Rats with hypertension showed an elevated blood pressure (BP), left ventricular functions, ang II, and decreased cGMP concentration of tissues. Treatment of chrysin is reverse to near normal in left ventricular functions, Ang-II, Ho-1 and decreased cGMP concentration of tissues. The antihypertensive effect of chrysin appears to be mediated by a reduction in left ventricular functions, cardiac oxidative stress and Ang-II, an increase in cardiac HO-1, cGMP concentration and a prevention of plasma nitric oxide loss.

Highlights

  • Hypertension and its related conditions as like as coronary artery disease, stroke, heart failure, and chronic renal failure is a growing public health issue for which successful treatment often remains inadequate [1]

  • The systolic contractility of the isolated heart was measured by the first temporal derivative of the left ventricular pressure (LVP) positive development (?dP/ dt, in mmHg/s), and the isovolumetric relaxation was measured by the first temporal derivative of the LVP negative pressure (- dP/dt, in mmHg/s)

  • A significant elevation of cardiac Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity was observed in the L-NAME group

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Summary

Introduction

Hypertension and its related conditions as like as coronary artery disease, stroke, heart failure, and chronic renal failure is a growing public health issue for which successful treatment often remains inadequate [1]. Cardiovascular diseases including hypertension are often associated with behavioural alterations. Hypertension is an over whelming global challenge, which ranks third as a means of reduction in disability-adjusted life-years [2]. Reactive oxygen species (ROS) have been shown to be critical determinants in hypertension. The contribution of oxidative stress to the pathogenesis of hypertension is supported to rely upon inactivation of the NO [3]. Renin–angiotensin system (RAS) plays a vital role in the regulation of vascular function and blood pressure [4]. Chronic NO inhibition with Nx-nitro-L-arginine methyl ester (L-NAME) can increase regional vascular resistance, raise the blood

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