Mild chronic renal insufficiency induces sympathetic overactivity

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Abstract
The objectives of this study were to evaluate baseline sympathetic nerve activity as well as the mechanisms of sympathetic overactivity in mild chronic renal insufficiency hypertension. Seven hypertensives with mild renal insufficiency, seven hypertensives with normal renal function and seven normotensives, age and weight-matched were studied on one session to evaluate baseline muscle sympathetic nerve activity measured in the peroneal nerve. The mild renal insufficiency hypertensives and the hypertensives with normal renal function were also studied to evaluate arterial baroreflex control of muscle sympathetic nerve activity assessed by increasing and decreasing blood pressure through continuous infusion of phenylephrine and sodium nitroprusside respectively. Baseline muscle sympathetic nerve activity was significantly higher in mild renal insufficiency hypertensives (34 bursts/min) when compared to hypertensives with normal renal function (24 bursts/min) and to normotensives (16 bursts/min). Baroreflex control of muscle sympathetic nerve activity was (in absolute values) 15.2 in hypertensives with normal renal function vs 2.6 in mild renal insufficiency hypertensives (P < 0.05) during phenylephrine and 6.3 vs 8.2 during nitroprusside infusions. Mild renal insufficiency hypertensives showed sympathetic overactivity when compared to hypertensives with normal renal function and to normotensives. This finding demonstrates that elevated sympathetic activity may be precociously detected in renal insufficiency. Baroreflex gain to phenylephrine was blunted in mild renal insufficiency hypertensives when compared to hypertensives with normal renal function, suggesting that bradycardic response in mild renal insufficiency is blunted.