Role of potassium channels in catecholamine secretion in the rat adrenal gland

Abstract

We elucidated the functional contribution of K+ channels to cholinergic control of catecholamine secretion in the perfused rat adrenal gland. The small-conductance Ca2+-activated K+ (SKCa)-channel blocker apamin (10–100 nM) enhanced the transmural electrical stimulation (ES; 1–10 Hz)- and 1,1-dimethyl-4-phenyl-piperazinium (DMPP; 5–40 μM)-induced increases in norepinephrine (NE) output, whereas it did not affect the epinephrine (Epi) responses. Apamin enhanced the catecholamine responses induced by acetylcholine (6–200 μM) and methacholine (10–300 μM). The putative large-conductance Ca2+-activated K+ channel blocker charybdotoxin (10–100 nM) enhanced the catecholamine responses induced by ES, but not the responses induced by cholinergic agonists. Neither the KA channel blocker mast cell degranulating peptide (100–1000 nM) nor the KV channel blocker margatoxin (10–100 nM) affected the catecholamine responses. These results suggest that SKCa channels play an inhibitory role in adrenal catecholamine secretion mediated by muscarinic receptors and also in the nicotinic receptor-mediated secretion of NE, but not of Epi. Charybdotoxin-sensitive Ca2+-activated K+ channels may control the secretion at the presynaptic site.