Interaction of SKCa channels and L-type Ca 21 channels in catecholamine secretion in the rat adrenal gland

نویسندگان

  • TAKAHIRO NAGAYAMA
  • YASUO FUKUSHIMA
  • HIROHIKO HIKICHI
  • MAKOTO YOSHIDA
  • MIZUE SUZUKI-KUSABA
  • HIROAKI HISA
  • TOMOHIKO KIMURA
  • SUSUMU SATOH
  • Tomohiko Kimura
چکیده

Nagayama, Takahiro, Yasuo Fukushima, Hirohiko Hikichi, Makoto Yoshida, Mizue Suzuki-Kusaba, Hiroaki Hisa, Tomohiko Kimura, and Susumu Satoh. Interaction of SKCa channels and L-type Ca 21 channels in catecholamine secretion in the rat adrenal gland. Am J Physiol Regulatory Integrative Comp Physiol 279: R1731–R1736, 2000.—We elucidated the interaction of small-conductance Ca-activated K (SKCa) channels and L-type Ca channels in muscarinic receptor-mediated control of catecholamine secretion in the isolated perfused rat adrenal gland. The muscarinic agonist methacholine (10–300 mM) produced concentration-dependent increases in adrenal output of epinephrine and norepinephrine. The SKCa channel blocker apamin (1 mM) 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 Ca channel blocker nifedipine (3 mM) or Ca-free solution. Nifedipine did not affect the methacholine-induced catecholamine responses, but it inhibited the responses during treatment with apamin. The L-type Ca channel activator Bay k 8644 (1 mM) 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 SKCa channels are activated by muscarinic receptor stimulation, which inhibits the opening of L-type Ca channels and thereby attenuates adrenal catecholamine secretion.

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تاریخ انتشار 2000