Role of the renal nerves in the pathogenesis of one-kidney renal hypertension in the rat.

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Abstract
Increased sympathetic nervous system activity has been demonstrated in established one-kidney one clip hypertension in the rat. To determine the importance of the renal nerves in this model of hypertension, renal denervation or sham operation was carried out 2 weeks after clipping. Systolic blood pressure (BP) after clipping the renal artery in 27 uninephrectomized male Charles River rats increased significantly from 125 +/- 3 mm Hg to a stable level of 185 +/-7 mm Hg by 2 weeks, in association with a positive sodium balance. Renal denervation in 13 animals resulted in a significant decrease in BP to 137 +/- 7 mm Hg, while no change in BP was seen after sham operation in 14 animals. There was no difference in mean daily water intake, mean daily sodium intake, mean daily urine volume, or mean fractional urinary sodium excretion between sham-operation and renal-denervated animals during the 2 weeks after operation. Plasma renin activity (PRA) and creatinine clearance were not significantly different at sacrifice 2 weeks after operation. Six of the renal-denervated rats were followed for 11 weeks after surgery. The BP rose again to hypertensive levels (187 +/- 8 mm Hg) by 5 weeks after renal denervation. Repeat renal denervation resulted in a significant decrease to 142 +/- 8 mm Hg. Renal denervation in eight rats with established one-kidney Grollman hypertension (185 +/- 8 mm Hg) also resulted ina significant decrease in systolic BP (143 +/- 8 mm Hg). The data demonstrate the importance of intact renal nerves in the maintenance of hypertension in the one-kidney renal hypertensive rat. The depressor effect of renal denervation is not mediated by alterations in sodium intake or excretion, water intake or excretion, creatinine clearance or PRA.