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,/?<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. {Hypertension 1991;18:805-812) I t has been widely observed that systemic hypertension in persons of African descent confers a considerably higher relative risk (four to six times) for the development of end-stage renal disease (ESRD) when compared with a white hypertensive population, 1 -4 even when blood pressure is "adequately" controlled. 56 The greater propensity for ESRD to develop in blacks as a consequence
The mechanisms responsible for increased blood pressure in response to a high dietary sodium intake in salt-sensitive patients with essential hypertension are only partially understood. The possibility that increased reactivity to pressor hormones might contribute to hypertension in these patients has not been adequately investigated. We studied 11 salt-sensitive and 15 salt-resistant patients with essential hypertension while they were ingesting a diet with 20 meq/day sodium for 9 days or one with 200 meq/day sodium for 14 days. During the last 4 days of each dietary regimen, they received 30 mg/day of slow-release nifedipine. Blood pressure response to increasing doses of norepinephrine and angiotensin II (Ang II) was studied at the end of each of four phases of the study. Salt-sensitive patients exhibited a greater blood pressure response to norepinephrine than salt-resistant patients, irrespective of the dietary sodium intake and whether we took into account the dose infused or the actual plasma levels of norepinephrine achieved during the infusion. The blood pressure response to Ang II, on the other hand, was greater in salt-sensitive than salt-resistant patients during low but not during high sodium intake. The blood levels of norepinephrine achieved during the infusion of this hormone were lower in salt-sensitive than in salt-resistant patients. These studies indicate that an increased reactivity to the pressor action of norepinephrine might contribute to the maintenance of hypertension in salt-sensitive patients. The increased reactivity appears to be specific for norepinephrine. In fact, we observed increased reactivity to Ang II during low but not during high sodium intake. Because salt-sensitive patients usually display suppressed levels of renin, the greater pressor response to Ang II during low sodium diet could be due to upregulation of Ang II receptors. Our studies also point to substantial differences in norepinephrine metabolism between salt-sensitive and salt-resistant patients with essential hypertension. P atients with essential hypertension display a great variability in their blood pressure response to a sodium load. Kawasaki et al 1 were the first to classify patients with essential hypertension as salt sensitive (SS) or salt resistant (SR) based on their blood pressure response to a sodium load, a finding confirmed by several other laboratories. 2 " 8 However, because the blood pressure changes in response to high sodium (Na + ) intake follow a Gaussian distribution, 3 any subdivision of hypertensive patients according to this criterion is arbitrary. Nonetheless, pathophysiological and clinical considerations still justify a classification of SS and SR hypertensive patients. We have classified as SS
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