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Prostaglandin release mediates drug‐induced stimulation of sodium transport in frog skin: the effects of quinacrine
Author(s) -
Erlij David,
Gersten Lewis
Publication year - 1985
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1985.tb11075.x
Subject(s) - frog skin , stimulation , pharmacology , prostaglandin , drug , chemistry , prostaglandin analogue , sodium , medicine , endocrinology , biochemistry , organic chemistry
1 Quinacrine markedly increased the release of prostaglandin E 2 (PGE 2 ) 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. 2 Quinacrine increased the amiloride‐sensitive short circuit current from 20.7 ± 2.1 μA cm −2 to 45.4 ± 6.5 μA cm −2 . 3 The stimulatory effects of quinacrine on both short circuit current and prostaglandin release were blocked in skins pretreated with indomethacin (10 −6 M). 4 Quinacrine did not block either the stimulation of the short circuit current or the increase in PGE 2 release caused by the calcium ionophore, ionomycin. 5 These results suggest: (a) the release of PGE 2 and the stimulation of the short circuit current caused by quinacrine are linked since blocking PGE 2 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 phosopholipases. 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 PGE 2 .