Reduced natriuretic response to increased renal interstitial hydrostatic pressure in Dahl salt-sensitive rats during volume expansion.

Abstract

Renal interstitial hydrostatic pressure (RIHP) plays a key role in the link between renal hemodynamics and the rate of the tubular reabsorption of sodium and water. Our objective was to determine whether the natriuretic response to a rise in RIHP induced by acute saline infusion would be altered in prehypertensive, Dahl salt-sensitive (DS) rats. We compared the effects of an acute saline load (2.5 ml/100 g BW over 30-min) on RIHP and urinary sodium excretion in Dahl salt-resistant (DR) (n = 11) and DS rats (n = 11) maintained from birth on a low-sodium diet. Baseline mean arterial pressure, glomerular filtration rate rate, and urinary sodium excretion did not differ between DR and prehypertensive DS rats. Urine flow rate and urinary sodium excretion increased significantly in both groups following saline loading. Increases were significantly (p < 0.05) less in the prehypertensive DS rats (0.32 +/- 0.07 to 3.62 +/- 0.79 microEq/min) than in the DR rats (0.71 +/- 0.22 to 6.30 +/- 1.35 microEq/min). RIHP also increased significantly in both groups, but did not differ significantly in DR (7.3 +/- 1.1 to 9.7 +/- 1.7 mmHg) vs. DS rate (7.9 +/- 1.0 to 9.8 +/- 1.3 mmHg). At an equal mean arterial pressure, DS rats showed a reduced natriuretic capacity after an acute saline load, prior to the development of hypertension. Renal tubular sensitivity to the increased RIHP that was induced by an acute saline load was blunted in prehypertensive DS rats.