This study was designed to test the hypothesis that a reduced number of nephrons from birth leads to increased arterial pressure in adulthood. Newborn Sprague-Dawley rat pups were uninephrectomized during the first 24 h after birth. In chronically instrumented adult animals (~22 wk), mean arterial pressure on a normal (0.20%)-Na⁺ diet was higher in uninephrectomized rats (133 ± 2 mmHg vs. 121 ± 2 mmHg in controls, P < 0.0001). Body weights were not significantly different, but the total kidney-to-body weight ratio was significantly reduced by 14% in adult uninephrectomized animals (P < 0.05). Glomerular filtration rate was reduced by ~30% in uninephrectomized rats (1.84 ± 0.09 vs. 2.63 ± 0.14 ml/min, P < 0.0002), and effective renal plasma flow was reduced to a lesser degree (6.37 ± 0.38 vs. 7.87 ± 0.51 ml/min, P < 0.03), such that the filtration fraction was also reduced (0.291 ± 0.007 vs. 0.338 ± 0.014, P < 0.01). After 7-10 days on a high (3.15%)-Na⁺ diet, arterial pressure increased more in uninephrectomized animals than in controls (20 ± 3 vs. 1 ± 1 mmHg, P < 0.003). Thus surgical removal of 50% of the nephrons, when done during development, caused reduced renal function and a salt-sensitive hypertension in adulthood. These data suggest that a reduced nephron endowment from birth, caused by genetic and/or perinatal environmental factors, could contribute to essential hypertension in adulthood.

kidney; glomerular filtration rate; renal plasma flow; salt sensitivity; development

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