Renal effects of rilmenidine in anesthetized rats: importance of renal nerves.

Renal function studies using standard clearance techniques were done in control and rilmenidine-infused (20 micrograms/Kg/min i.v. for 80 min) Wistar rats anesthetized with Inactin. The role of renal sympathetic nerves in the action of rilmenidine was assessed using rats in which the left kidney was denervated 7 to 10 days before the experiment. In other experiments, renal sympathetic nerve activity was recorded during infusion of rilmenidine. Arterial pressure and heart rate were decreased significantly by rilmenidine but changes in arterial pressure were limited to 10 to 12 mm Hg by ligating the proximal aorta during infusion of rilmenidine. Under these conditions, rilmenidine did not alter glomerular filtration rate significantly, but renal blood flow increased significantly in both innervated and denervated kidneys. Urine flow, total and fractional sodium excretion, and clearance of osmoles increased significantly in innervated kidneys but not in denervated kidneys. Free water clearance was decreased significantly, but only in the innervated kidney. Potassium excretion and fractional potassium excretion were increased significantly in both kidneys, although the change was larger in the innervated kidneys. Rilmenidine decreased renal sympathetic nerve activity progressively until by 80 min nerve activity was essentially absent. The data indicate that rilmenidine increases renal blood flow and potassium excretion by a mechanism independent of renal nerves, whereas the natriuresis and diuresis is dependent upon intact renal nerves. The increase in fractional excretion of sodium was associated with a marked decrease in renal sympathetic nerve activity suggesting that the natriuresis is caused by decreased tubular reabsorption of sodium subsequent to a central action of rilmenidine.