AJP - Renal Physiology, Vol 245, Issue 1 48-F57, Copyright © 1983 by American Physiological Society
Effects of fluid intake on basal and vasopressin-responsive urinary prostaglandin E
H. T. Campbell, P. A. Craven and F. R. DeRubertis
The effects of fluid intake on basal and vasopressin-responsive urinary PGE
excretion (UPGEV) were examined in conscious rats under conditions of 1) ad
libitum water intake, 2) water deprivation, and 3) water diuresis induced
by ad libitum intake of 5% dextrose in water. UPGEV fell progressively
during 40 h of water deprivation. Water diuresis after water deprivation
increased UPGEV transiently (8 h). Vasopressin (Pitressin tannate in oil, 5
U/kg subcutaneously) increased UPGEV and decreased urine volume (V) in rats
on ad libitum water intake but did not alter UPGEV during water
deprivation. Indomethacin suppressed UPGEV (70-90%), increased basal urine
osmolality (Uosmol), and potentiated the antidiuretic response to Pitressin
in rats on ad libitum water intake. Indomethacin accelerated by 8 h the
onset of maximal antidiuresis in water-deprived rats but did not
significantly alter water balance. During water diuresis, UPGEV declined in
the first 8 h after Pitressin. Thereafter, UPGEV increased markedly,
concurrent with early vasopressin escape. Indomethacin or meclofenamate
inhibited the rise in UPGEV, the decline in Uosmol, and the increase in V
of the escape phase. Indomethacin or meclofenamate also impaired the
excretion of an acute water load (5% body wt) given during escape. The
spontaneous decline in UPGEV during hydropenia may serve to maximize
physiologic antidiuresis. Conversely, the marked increase in UPGEV induced
by administration of vasopressin during water diuresis may serve to
suppress the antidiuretic response and thus play a role in the mediation of
escape from physiologically inappropriate antidiuresis.
