抄録
Vasopressin-prostaglandin (PG) interaction, especially the role of the inhibitory effects of PGE2 on vasopressin action, was studied using toad urinary bladders. The PGH2, at 1×10-7M, inhibited vasopressin-stimulated water flow (MARUMO, 1982); PGE2 inhibited the water flow at 10-8M, but PGD2, PGF2α, and PGI2 did not do so even at 10-7M. Thus, PGE2 has a physiological effect in contrast to other PGs converted from PGH2. Indomethacin enhanced both the vasopressin- and cyclic AMP-stimulated water flow across the toad bladder. However, the half maximum activation dose for vasopressin was 2×10-10M, but for cyclic AMP, as much as 3×10-8M. The PGE2 inhibited both vasopressin- and cyclic AMP-stimulated water flow. However, PGE2 inhibited vasopressin action in a dose-dependent manner which was not noted as a PGE2 effect on cyclic AMP action. The W-7, which is a specific inhibitor of calmodulin, suppressed cyclic AMP-stimulated water flow in a dose-dependent manner. Thus, PGE2 may suppress vasopressin-stimulated water flow at a site of cyclic AMP generation under physiological conditions. Thromboxane B2 (TXB2) enhanced vasopressin-stimulated water flow but not cyclic AMP-stimulated one. Thus PGE2 and TXB2 may be concluded as negative or positive modulators of vasopressin action in the toad bladder on the step(s) as the site of cyclic AMP generation under physiological conditions.
