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

Takahiro Nagayama, Yasuo Fukushima, Makoto Yoshida, Mizue Suzuki-Kusaba, Hiroaki Hisa, Tomohiko Kimura, Susumu Satoh

Research output: Contribution to journalArticle

8 Citations (Scopus)

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+ (SK(Ca))-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 K(A) channel blocker mast cell degranulating peptide (100-1000 nM) nor the K(V) channel blocker margatoxin (10-100 nM) affected the catecholamine responses. These results suggest that SK(Ca) 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.

Original languageEnglish
Pages (from-to)R448-R454
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume279
Issue number2 48-2
DOIs
Publication statusPublished - 2000 Jan 1

Keywords

  • Apamin
  • Charybdotoxin
  • K(A) channel
  • K(V) channel
  • Large-conductance Ca-activated K
  • Margatoxin
  • Mast cell degranulating peptide
  • Small-conductance Ca-activated K

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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