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Emblica officinalis Exerts Antihypertensive Effect in a Rat Model of DOCA-Salt-Induced Hypertension: Role of (p) eNOS, NO and Oxidative Stress

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Abstract

Emblica officinalis (EO) has antioxidant properties that could improve redox-sensitive vascular, cardiac and renal changes associated with deoxycorticosterone acetate/1% NaCl high salt (DOCA/HS)-induced hypertension. We determined whether hydroalcoholic lyophilized extract of EO may influence DOCA/HS-induced hypertension by modulating activity of (p) eNOS and endogenous antioxidants. Hypertension was induced in rats by DOCA-salt (20 mg/kg, s.c.) twice weekly for 5 weeks and replacing drinking water with 1% NaCl solution. These rats received cotreatment of different doses of EO (75, 150 and 300 mg/kg/day) for 5 weeks. EO significantly decreased arterial blood pressure and heart rate along with cardiac and renal hypertrophy in a dose-dependent fashion as compared to DOCA control rats. Increased TBARS and decreased endogenous antioxidants including GSH, SOD and GSHPx activity in serum, heart and kidney tissues of hypertensive rats were also normalized. Furthermore, this antihypertensive activity of EO was also linked with increased serum NO, K+ levels and decreased Na+ levels. Moreover, EO robustly increased activated eNOS expression in heart. Our results demonstrate that EO reduces oxidative stress, prevents development and progression of hypertension as well as cardiac and renal hypertrophy in DOCA/HS-induced hypertension via modulation of activated eNOS, endogenous antioxidants, serum NO and electrolyte levels.

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Acknowledgments

This study was supported by a grant from institutional funding agency, AIIMS, New Delhi-110029, India. We are thankful to Sanat product limited, New Delhi, India, for kindly providing hydroalcoholic lyophilized extract of Emblica officinalis as a gift sample.

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Correspondence to Jagriti Bhatia.

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Bhatia, J., Tabassum, F., Sharma, A.K. et al. Emblica officinalis Exerts Antihypertensive Effect in a Rat Model of DOCA-Salt-Induced Hypertension: Role of (p) eNOS, NO and Oxidative Stress. Cardiovasc Toxicol 11, 272–279 (2011). https://doi.org/10.1007/s12012-011-9122-2

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