Tonic and reflex control of renal sympathetic nerve activity are altered by a discrete increase in sodium intake in renovascular hypertensive rats

Abstract

Sympathoexcitation and baroreceptor dysfunction are involved in the pathophysiology of renovascular hypertension (2K1C). In the present study we investigated the effects of a discrete increase in sodium intake in 2K1C rats. Animals were divided in 4 independent groups (n=± 6/group) and treated for 2 weeks with normal sodium diet (0.5% NNa+) or high sodium diet (2% HNa+) after 4 weeks of renovascular hypertension. Water intake (WI) and urinary volume (UV) was increased in 2K1C HNa+ compared to 2K1C NNa+ (WI 2K1C HNa+ 61.1±6.4 2K1C; NNa+39.8±2.5; mL/day); UV (2K1C HNa+ 50 ± 5 mL/day; NNa+ 25.4±2.3; 2K1C). Arterial blood pressure (ABP) was significantly increased in 2K1C compared only to control group (2K1C NNa+ 174 ± 5; control NNa+ 100 ± 3 mmHg). Increased sodium intake enhanced the baroreflex sensitivity gain of HR in control and 2K1C (control NNa+ −2.6±0.7; control HNa+−5.3±0.4; 2K‐1C NNa+ −1.7±0.2; 2K‐1C HNa+ −4.1±0.6 bpm/mmHg). Renal sympathetic nerve activity (RSNA) gain was enhanced only in 2K1C HNa+(2K1C NNa+ −0.7±0.03; 2K1C HNa+ −1.4±0.06 pps/mmHg). Our results suggest that in the renovascular hypertension the improvement in the baroreceptor sensitivity to the kidney is probably a mechanism leading to increased diuresis avoiding further increase in ABP.Supported by FAPESP, CNPq