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Division of Nephrology, Hypertension, and Clinical Pharmacology, Oregon Health Sciences University, Portland, Oregon 97201-3098
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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