AJP - Renal Physiology, Vol 246, Issue 1 32-F38, Copyright © 1984 by American Physiological Society
Efferent role of ADH in CNS-induced natriuresis
E. T. Pierce, R. J. Grekin and D. R. Mouw
Ventriculocisternal perfusion (VCP) of artificial cerebrospinal fluid (CSF)
was performed in pentobarbital-anesthetized dogs. Renal function was
studied in protocols consisting of a 1-h experimental period in which the
animals received either CSF with an elevated sodium concentration (300 mM,
high Na) via VCP or antidiuretic hormone (ADH) intravenously, bracketed by
1-h control and recovery periods. High Na VCP caused an increase in plasma
ADH measured by radioimmunoassay (to 176% of control) that coincided with a
natriuresis (to 180% of control). In a second set of experiments, these
changes in endogenous ADH were mimicked experimentally with intravenous
infusions of synthetic ADH in animals receiving continuous VCP with normal
sodium artificial CSF. The dose-response relationship between log ADH and
urinary sodium excretion for the intravenous ADH experiments was not
different from the relationship for those experiments in which ADH was
elevated as a consequence of high Na VCP. These results suggest that ADH
causes part, if not all, the natriuresis induced by high Na VCP.
