Interaction of SK(Ca) channels and L-type Ca2+ channels in catecholamine secretion in the rat adrenal gland

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

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)


We elucidated the interaction of small-conductance Ca2+-activated K+ (SK(Ca)) channels and L-type Ca2+ channels in muscarinic receptor-mediated control of catecholamine secretion in the isolated perfused rat adrenal gland. The muscarinic agonist methacholine (10-300 μM) produced concentration-dependent increases in adrenal output of epinephrine and norepinephrine. The SK(Ca) channel blocker apamin (1 μM) enhanced the methacholine-induced catecholamine responses. The facilitatory effect of apamin on the methacholine-induced catecholamine responses was not observed during treatment with the L-type Ca2+ channel blocker nifedipine (3 μM) or Ca2+-free solution. Nifedipine did not affect the methacholine-induced catecholamine responses, but it inhibited the responses during treatment with apamin. The L-type Ca2+ channel activator Bay k 8644 (1 μM) enhanced the methacholine-induced catecholamine responses, whereas the enhancement of the methacholine-induced epinephrine and norepinephrine responses were prevented and attenuated by apamin, respectively. These results suggest that SK(Ca) channels are activated by muscarinic receptor stimulation, which inhibits the opening of L-type Ca2+ channels and thereby attenuates adrenal catecholamine secretion.

Original languageEnglish
Pages (from-to)R1731-R1736
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Issue number5 48-5
Publication statusPublished - 2000


  • Adrenal catecholamine
  • Apamin
  • Bay k 8644
  • Muscarinic receptors
  • Nifedipine

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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