Endogenous prostaglandins, adenosine 3':5'‐monophosphate and sodium transport across isolated frog skin.

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Abstract
Na transport across isolated frog skin, as measured by the short-circuit current [SCC], was decreased by acetylsalicylic acid [AA], mefenamic acid, paracetamol [Pa] and phenylbutazone. Indomethacin [Im] (6 .times. 10-6 M) had a biphasic effect on the SCC: a transient increase followed by a sustained decrease. The release of prostaglandin[G]-like material from the skin was reduced by AA and Im. Pa caused a significant reduction in the SCC response of the skin to low doses of arachidonic acid, but the response to the highest dose tested was not significantly altered. Im (6 .times. 10-6 M) increased the sensitivity of the skin to applied PGE1. The other prostaglandin synthetase inhibitors did not have this effect. Im (6 .times. 10-6 M) also enhanced the effect of antidiuretic hormone on the SCC. Im (30 .times. 10-6 M) increased the SCC and diminished the response to applied PGE1. In sulfate Ringer, theophylline [T] increased the SCC and diminished the response to PGE1. PGE1 increased the levels of cyclic[c]AMP in frog skin and these increases preceded the increases in SCC. There was a seasonal variation in the level of cAMP levels in the skin; the levels in winter exceeded those in summer. There was also a seasonal variation in cAMP response to PGE1; the winter response was greater than that in summer. Im (6 .times. 10-6 M) had a biphasic effect on cAMP levels in the skin, an initial increase followed by a decrease. Im also potentiated PGE1-stimulated cAMP accumulation. T increased cAMP levels in the skin and potentiated PGE1-stimulated cAMP accumulation.