Fukushima Yasuo, Nagayama Takahiro, Hikichi Hirohiko, Mizukami Kazuhiko, Yoshida Makoto, Suzuki-Kusaba Mizue, Hisa Hiroaki, Kimura Tomohiko, Satoh Susumu
Laboratory of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Aobayama, 980-8578, Sendai, Japan.
Eur J Pharmacol. 2002 Feb 15;437(1-2):69-72. doi: 10.1016/s0014-2999(02)01275-x.
We eluciated whether K+ channels modulate adrenal catecholamine secretion induced by pituitary adenylate cyclase-activating polypeptide (PACAP) in the isolated perfused rat adrenal gland. PACAP (100 nM) increased adrenal epinephrine output. The PACAP-induced responses were enhanced by treatment with apamin (10-100 nM) in a concentration-dependent manner. In the presence of nifedipine (3 microM), apamin (1 microM) did not enhance the PACAP-induced responses. Charybdotoxin (1-100 nM) had little influence on the PACAP-induced responses. These results suggest that small-conductance Ca2+-activated K+ channels interfere with L-type voltage-dependent Ca2+ channels to counteract the PACAP-induced adrenal catecholamine secretion.
我们阐明了在离体灌注的大鼠肾上腺中，钾离子通道是否调节垂体腺苷酸环化酶激活多肽（PACAP）诱导的肾上腺儿茶酚胺分泌。PACAP（100 nM）增加了肾上腺肾上腺素的输出。阿帕明（10 - 100 nM）以浓度依赖性方式增强了PACAP诱导的反应。在硝苯地平（3 microM）存在的情况下，阿帕明（1 microM）并未增强PACAP诱导的反应。蝎毒素（1 - 100 nM）对PACAP诱导的反应影响很小。这些结果表明，小电导钙激活钾通道干扰L型电压依赖性钙通道，以抵消PACAP诱导的肾上腺儿茶酚胺分泌。
