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

We elucidated the functional contribution of K+ channels to cholinergic con trol of catecholamine secretion in the perfused rat adrenal gland. The smal l-conductance Ca2+-activated K+ (SKCa)-channel blocker apamin (10-100 nM) e nhanced the transmural electrical stimulation (ES; 1-10 Hz)- and 1,1-dimeth yl-4-phenyl-piperazinium (DMPP; 5-40 mu M)-induced increases in norepinephr ine (NE) output, whereas it did not affect the epinephrine (Epi) responses. Apamin enhanced the catecholamine responses induced by acetylcholine (6-20 0 mu M) and methacholine (10-300 mu M). The putative large-conductance Ca2-activated K+ channel blocker charybdotoxin (10-100 nM) enhanced the catech olamine responses induced by ES, but not the responses induced by cholinerg ic agonists. Neither the K-A channel blocker mast cell degranulating peptid e (100-1000 nM) nor the K-V 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 muscarin ic receptors and also in the nicotinic receptor-mediated secretion of NE, b ut not of Epi. Charybdotoxin-sensitive Ca2+-activated K+ channels may contr ol the secretion at the presynaptic site.