Antihypertensive and Bilateral Renal Responses to Nifedipine in 2-Kidney, 1-Clip, Goldblatt Hypertensive Rats

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Abstract
Experiments were performed to assess the effects of nifedipine, a calcium channel blocker, on the blood pressure and bilateral renal function in 2-kidney, 1-clip, Goldblatt hypertensive rats. Hypertensive rats were prepared 4 weeks prior to the acute experiments. Nifedipine was administered intravenously into hypertensive (n = 11) and control (n = 12) rats under pentobarbital anesthesia. In hypertensive rats, nifedipine (0.02 mg/kg) reduced the mean arterial pressure from 151 ± 5 to 135 ± 5 mm Hg. Despite the fall of arterial pressure, there were significant increases in glomerular filtration rate (GFR) from 1.36 ± 0.13 to 1.80 ± 0.22 ml/min, urine flow from 7.8 ± 1.6 to 17.0 ± 3.8 µl/min, and excretions of absolute and fractional sodium from 1.07 ± 0.43 µEg/min and 0.50 ± 0.15% to 2.80 ± 0.73 µEq/min and 0.92 ± 17%, respectively, in the nonclipped kidney. No significant changes in these renal indices occurred in the clipped kidney. In control rats, administration of nifedipine (0.04 mg/kg) also significantly decreased the arterial pressure from 119 ± 4 to 110 ± 4 mm Hg. There were slight but insignificant increases in GFR and renal excretion of sodium and water. In both groups, nifedipine produced proportionate increases in osmolar clearance and free water reabsorption. These results suggest that nifedipine enhances glomerular filtration and suppresses the reabsoption of sodium and water by the proximal tubule and/or distal nephron segments. The resulting increase in excretory function of the nonclipped kidney may, in part, contribute to the blood pressure-lowering effect of this drug.