The antihypertensive effects of quercetin in a salt-sensitive model of hypertension.

Abstract

Salt-sensitive hypertension can be caused through abnormalities related to sodium and body fluid homeostasis; renin-angiotensin-aldosterone (RAAS) plays a key role in this regard. The molecular basis of the purported antihypertensive benefits of some plant-derived compounds such as quercetin is still lacking. To this end, we investigated RAAS in the Dahl salt-sensitive rat model with emphasis on the kidney. Eighteen rats were treated with captopril (CAP), quercetin (QUE), and dimethyl sulfoxide (controls) over a 4-week period. CAP and QUE lowered systolic blood pressure significantly in comparison to day 0 (baseline values). These findings were in keeping with their increased urinary output, increased sodium output, decreased aldosterone and decreased AT1a mRNA. QUE did not differ significantly from controls with regards to aldosterone levels. QUE was effective in lowering blood pressure in this model of hypertension, probably because of a modulation of renal function.