AJP - Renal Physiology, Vol 245, Issue 6 763-F771, Copyright © 1983 by American Physiological Society
CNS-induced natriuresis and renal hemodynamics in conscious rats
D. Beasley, R. L. Malvin and D. R. Mouw
Sodium excretion was studied following experimental elevation of
cerebrospinal fluid (CSF) sodium in heterozygous and homozygous (DI)
Brattleboro rats given exogeneous antidiuretic hormone. Sodium excretion
increased 4.5-fold in heterozygous and 3.5-fold in DI rats. The natriuresis
in both groups was rapid in onset and occurred with a simultaneous
kaliuresis. Blood pressure increased approximately 10 mmHg in the
heterozygous but not in the DI rats. Accordingly, increased blood pressure
may contribute to the natriuresis but is not the sole mechanism. Plasma
renin concentration did not change in the DI rats during high Na CSF
infusion, and chronic bilateral renal denervation did not abolish the
natriuresis. Glomerular filtration rate increased during the high Na period
in both the intact and renally denervated rats. These data provide evidence
that a natriuretic mechanism exists that is not mediated by changes in
antidiuretic hormone, renal nerve activity, mean arterial pressure,
aldosterone, or angiotensin II, and thus may be due to another circulating
substance or natriuretic hormone. This hormone may act totally or in part
by increasing glomerular filtration rate.
