Renal interstitial hydrostatic pressure during verapamil-induced natriuresis

Abstract

Infusion of calcium antagonists results in significant increases in sodium excretion, an effect that is exacerbated in hypertensive animals. The mechanism responsible for the increase in sodium excretion has not been elucidated. The purpose of this study was to determine the role of renal interstitial hydrostatic pressure (RIHP) in mediating increases in sodium excretion produced by the calcium antagonist verapamil. Changes in renal hemodynamics and electrolyte excretion were examined in response to an intrarenal infusion of verapamil (100 micrograms/min) in normal dogs and in dogs with angiotensin II-induced hypertension. Infusion of verapamil in normal dogs increased renal blood flow by 18% and had no effect on glomerular filtration rate. Renal vascular resistance and filtration fraction both decreased in response to verapamil. Absolute (5.1 +/- 2.3 to 176 +/- 45.8 mueq/min) and fractional excretion of sodium (0.21 +/- 0.13 to 7.36 +/- 3.12%) also increased significantly. Despite renal vasodilation, the natriuresis was not associated with significant increases in RIHP (6.4 +/- 0.9 to 5.8 +/- 0.9 mmHg). Infusion of verapamil into dogs with angiotensin II hypertension resulted in a natriuresis (4.2 +/- 1.6 to 338.7 +/- 78.3 mueq/min) that was much greater than under normal conditions. Although the renal vasodilation was significantly higher in the angiotensin II-hypertensive dogs, the enhanced natriuresis in these animals was not associated with increases in RIHP. The results of this study indicate that increases in RIHP are not responsible for the natriuresis produced by verapamil in normal or angiotensin II-hypertensive dogs.