Key result
Red wine polyphenols prevent angiotensin II-induced hypertension in rats by curbing vascular NADPH oxidase induction.
OBJECTIVE: Chronic administration of moderate amounts of red wine has been associated with a protective effect on the cardiovascular system. This study examined whether red wine polyphenols prevent the angiotensin II (Ang II)-induced hypertension and endothelial dysfunction in rats, and, if so, to elucidate the underlying mechanism. METHODS: Hypertensive rats were obtained by a 14-day infusion of Ang II. Red wine polyphenols were administered in the drinking water one week before and during the Ang II infusion. Arterial pressure was measured in conscious rats. Ex vivo vascular relaxation was assessed in organ chambers, vascular superoxide anion production by dihydroethidine and vascular NADPH oxidase expression by immunohistochemistry. RESULTS: Ang II-induced hypertension was associated with decreased relaxation to acetylcholine but not to red wine polyphenols. The Ang II treatment also increased vascular superoxide anion production and expression of nox1 and p22phox NADPH oxidase subunits. Intake of red wine polyphenols prevented the Ang II-induced hypertension and endothelial dysfunction and normalized vascular superoxide anion production and NADPH oxidase subunit expression. Red wine polyphenol treatment alone did not affect blood pressure. CONCLUSION: Intake of red wine polyphenols prevents Ang II-induced hypertension and endothelial dysfunction. Prevention of vascular NADPH oxidase induction and preservation of arterial nitric oxide availability during Ang II administration likely contribute to this effect.
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Sarr et al. (2006) studied Angiotensin II-induced hypertension and endothelial dysfunction. Red wine polyphenols vs. Angiotensin II infusion without red wine polyphenols was evaluated on Arterial pressure, ex vivo vascular relaxation, vascular superoxide anion production, and vascular NADPH oxidase expression. Intake of red wine polyphenols prevented angiotensin II-induced hypertension and endothelial dysfunction in rats, likely by preventing vascular NADPH oxidase induction.
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