AJP - Renal Physiology, Vol 250, Issue 6 1008-F1012, Copyright © 1986 by American Physiological Society
Increased PGE2 excretion by dDAVP in humans depends on state of hydration
U. Schwertschlag, J. G. Gerber, J. S. Barnes and A. S. Nies
The relationship of renal prostaglandin E2 (PGE2) excretion (UPGEV) to
water deprivation, water diuresis, and subsequent antidiuresis by
1-desamino-8-D-arginine vasopressin (dDAVP) was studied in female
volunteers. After 16 h of water deprivation, the subjects began a sustained
water diuresis for 8 h. This diuresis caused a transient twofold rise in
UPGEV at 2 h (P less than 0.05), which then fell back to or below baseline
levels. dDAVP given during the water diuresis caused a transient rise of
UPGEV as urine volume decreased and plasma osmolality fell from 277 +/- 1.5
to 271 +/- 2 mosmol/kg (P less than 0.01). Another group of subjects had
the water diuresis discontinued after 4 h with dDAVP given at the 5th h
when urine volume was decreasing and urine osmolality was increasing. In
this setting dDAVP did not produce as great a fall in plasma osmolality nor
did it increase UPGEV. These data indicate that renal prostaglandin
synthesis (as determined by UPGEV) is increased transiently by an acute
water load; dDAVP given during continued water ingestion results in a fall
in plasma osmolality and increased PGE excretion; however, dDAVP does not
increase UPGEV during normal hydration; and UPGEV is independent of changes
in urine flow. These findings imply that renal prostaglandins may have a
functional role in humans to inhibit the hydroosmotic actions of
antidiuretic hormone, and thus hasten the excretion of a water load, and to
prevent overhydration when inappropriate antidiuresis occurs. However,
there is no evidence that the stimulus for prostaglandin production is
dDAVP per se.
