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. 1985 Aug;85(4):775–781. doi: 10.1111/j.1476-5381.1985.tb11075.x

Prostaglandin release mediates drug-induced stimulation of sodium transport in frog skin: the effects of quinacrine.

D Erlij, L Gersten
PMCID: PMC1916656  PMID: 3876129

Abstract

Quinacrine markedly increased the release of prostaglandin E2 (PGE2) into the basolateral solution of the bullfrog skin from a control value of 32.7 +/- 21.7 pg per 20 min period to a stimulated value of 8593.1 +/- 4112.3 pg per 20 min period. Quinacrine increased the amiloride-sensitive short circuit current from 20.7 +/- 2.1 microA cm-2 to 45.4 +/- 6.5 microA cm-2. The stimulatory effects of quinacrine on both short circuit current and prostaglandin release were blocked in skins pretreated with indomethacin (10(-6) M). Quinacrine did not block either the stimulation of the short circuit current or the increase in PGE2 release caused by the calcium ionophore, ionomycin. These results suggest: (a) the release of PGE2 and the stimulation of the short circuit current caused by quinacrine are linked since blocking PGE2 release inhibits the stimulation of the short circuit current; (b) given the complexity of its actions, quinacrine is a poor tool to examine whether the effects of a given agent are mediated through the activation of endogenous phospholipases. In addition our results taken together with other findings in the literature suggest that there is a diverse group of compounds that stimulate transepithelial sodium transport by releasing PGE2.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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