This study was designed to test the hypothesis that a reduced number of nep
hrons 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 (similar to 22 wk, mean a
rterial pressure on a normal (0.20%)-Na+ diet was higher in uninephrectomiz
ed rats (133 +/- 2 mmHg vs. 121 +/- 2 mmHg in controls, P < 0.0001). Body w
eights were not significantly different, but the total kidney-to-body weigh
t ratio was significantly reduced by 14% in adult uninephrectomized animals
(P < 0.05). Glomerular filtration rate was reduced by similar to 30% in un
inephrectomized 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 w
as 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 unine
phrectomized animals than in controls (20 +/- 3 vs. 1 +/- 1 mmHg, P < 0.003
). Thus surgical removal of 50% of the nephrons, when done during developme
nt, caused reduced renal function and a salt-sensitive hypertension in adul
thood. These data suggest that a reduced nephron endowment from birth, caus
ed by genetic and/or perinatal environmental factors, could contribute to e
ssential hypertension in adulthood.