AJP - Renal Physiology, Vol 248, Issue 3 454-F458, Copyright © 1985 by American Physiological Society
Interactions of vasopressin, cAMP, and prostaglandins in toad urinary bladder
D. Schlondorff and J. A. Satriano
Prostaglandin (PG) inhibits the hydroosmotic effect of vasopressin. We
therefore reexamined the interaction of vasopressin (VP), cAMP, and
prostaglandins in toad bladder epithelial cells. Vasopressin slightly, but
reproducibly, stimulated PGE2 and thromboxane B2 (TXB2) synthesis in cells
prepared by the use of collagenase. When cells were prepared in the
presence of a readily reversible cyclooxygenase inhibitor, ibuprofen,
subsequent PGE2 synthesis was enhanced sevenfold but that of TXB2 was not.
Increasing cAMP by either phosphodiesterase inhibition or 8-bromo-cAMP
significantly inhibited both basal and VP-stimulated PGE2 synthesis. This
inhibition was overcome by addition of arachidonic acid. Future studies
employing these agents will have to consider these effects. VP enhanced 32P
labeling of phosphatidylinositol (PI) and phosphatidic acid. This effect
was prevented by the phosphodiesterase inhibitor, which also decreased
phosphatidylcholine labeling. The results indicate that the
phosphodiesterase inhibitor for cAMP may decrease PG formation by
interfering with phospholipase activation. Furthermore, VP, similar to its
effect in the liver, also increases PI turnover in toad bladder. This may
initiate PG synthesis and provide a link among VP, cAMP, and calcium. A
double-reciprocal feedback is proposed, whereby VP stimulates PG synthesis
in a cAMP-independent manner and also inhibits PG synthesis in a
cAMP-dependent manner.
