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The present study was attempted to investigate the effect of quinine on secretion of catecholamlnes(CA) evoked by cholinergic stimulation and membrane depolarization from the i solated perfused rat adrenal g1and. The perfusion of quinine (15-150mcM) into an adrenalveln for 60 min produced dose- and time-dependent inhibition in CA secretion evoked by Ach(5.32×103M), high K+(5.6x10-2M), DMPP (10-4M for 2 min), McN-A-343 (10-4 M for 2 min), cyclopiazonic acid (10-5M for 4 min) and Bay-K-8644 (107M thor 4 min). Also, under the presence of pinacidil (10-4,/sup> M), which is also known to be a selective potassiurm channel activator, CA secretory responses evoked by Ach, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also great1y reduced. When preloaded alone with quinine(5x10-5 M) and glibenclmide (10-6 M), a specific blocker of ATP-regulated potassium channels, CA secretory responses evoked by Ach, hlgh potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonlc aclu were recovered as compared to thole of quinine-treatment only. Taken together, these results demoustrate that quinine inhibits CA secretion evoked by stimulation of cholinergic(both nicotinic and muscellular) receptors as well as by membrane depolarization through inhibiting inf1ux of extracellular calclum arid release in intracellular calcium in the rat adrenomedullarv chromaffin cells. These findings suggest that activation of potassium channels may be involved at least in inhibitory actiono. Quinlne on CA secretion from the rat adrenal gland.
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