Abnormal renal hemodynamics in black salt-sensitive patients with hypertension

Abstract

African-Americans with essential hypertension are more prone to the development of renal failure and are frequently salt-sensitive as well. Because alterations of intrarenal hemodynamics are important in the progression of renal disease and because salt-sensitive animal models with hypertension manifest a greater propensity to develop glomerulosclerosis in association with a rise in glomerular capillary pressure, we tested whether the renal hemodynamic adaptation to high dietary Na+ intake differs in salt-sensitive and salt-resistant hypertensive patients. We studied 17 black and nine white patients with essential hypertension who were placed on a low Na+ diet (20 meq/day) for 9 days, followed by a high Na+ diet (200 meq/day) for 14 days. During the last 4 days of each diet regimen, they received 30 mg/day of slow-release nifedipine. Eleven blacks were salt-sensitive, and all whites were salt-resistant. During the low Na+ diet period, salt-sensitive and salt-resistant patients had similar mean arterial pressure, glomerular filtration rate, effective renal plasma flow, and filtration fraction. During the high Na+ intake period, glomerular filtration rate did not change in either group; effective renal blood flow increased in salt-resistant patients (from 455±25 to 524±27.7 ml/min, p<0.01), but it decreased in salt-sensitive patients (from 538±20 to 426±15.8 ml/min, p<0.01); filtration fraction decreased (from 21±1.8 to 19±1.5%) in salt-resistant patients, but it increased (from 19±0.9 to 23±1.5%, p<0.01) in salt-sensitive patients; glomerular pressure decreased (from 58±2.0 to 52±1.5 mm Hg, p<0.01) in salt-resistant patients, but it increased (from 48±1.6 to 58±1.5 mm Hg, p<0.01) in salt-sensitive patients. During the period of high Na+ intake, nifedipine decreased arterial pressure, renal vascular resistance, and filtration fraction and increased renal blood flow in salt-sensitive but not in salt-resistant patients. These studies show that an abnormal renal hemodynamic adaptation occurs in salt-sensitive patients during high Na+ intake. The rise in filtration fraction and in intraglomerular pressure during high Na+ suggests that these renal hemodynamic derangements might be partially responsible for the greater propensity to renal failure in hypertensive African-Americans.