Nagayama T, Masada K, Yoshida M, Suzuki-Kusaba M, Hisa H, Kimura T, Satoh S
Department of Pharmacology, Tohoku University, Sendai, Japan.
Am J Physiol. 1998 Apr;274(4):R1125-30. doi: 10.1152/ajpregu.1998.274.4.R1125.
We examined the role of K+ channels in the secretion of adrenal catecholamine (CA) in response to splanchnic nerve stimulation (SNS), acetylcholine (ACh), 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. K+ channel blockers and the cholinergic agonists were infused and injected, respectively, into the adrenal gland. The voltage-dependent K+ channel (KA type) blocker mast cell degranulating (MCD) peptide infusion (10-100 ng/min) enhanced increases in CA output induced by SNS (1-3 Hz), but it did not affect increases in CA output induced by ACh (0.75-3 micrograms), DMPP (0.1-0.4 microgram), or muscarine (0.5-2 micrograms). The small-conductance Ca(2+)-activated K+ (SKCa) channel blocker scyllatoxin infusion (10-100 ng/min) enhanced the ACh-, DMPP-, and muscarine-induced increases in CA output, but it did not affect the SNS-induced increases in CA output. These results suggest that KA channels may play an inhibitory role in the regulation of adrenal CA secretion in response to SNS and that SKCa channels may play the same role in the secretion in response to exogenously applied cholinergic agonists.
我们研究了钾通道在麻醉犬体内，对内脏神经刺激（SNS）、乙酰胆碱（ACh）、1,1 - 二甲基 - 4 - 苯基哌嗪鎓（DMPP）和毒蕈碱作出反应时，肾上腺儿茶酚胺（CA）分泌中的作用。分别将钾通道阻滞剂和胆碱能激动剂注入和注射到肾上腺中。电压依赖性钾通道（KA型）阻滞剂肥大细胞脱颗粒（MCD）肽注入（10 - 100纳克/分钟）增强了由SNS（1 - 3赫兹）诱导的CA输出增加，但不影响由ACh（0.75 - 3微克）、DMPP（0.1 - 0.4微克）或毒蕈碱（0.5 - 2微克）诱导的CA输出增加。小电导钙激活钾（SKCa）通道阻滞剂刺尾鱼毒素注入（10 - 100纳克/分钟）增强了由ACh、DMPP和毒蕈碱诱导的CA输出增加，但不影响由SNS诱导的CA输出增加。这些结果表明，KA通道可能在对SNS作出反应时肾上腺CA分泌的调节中起抑制作用，而SKCa通道可能在外源性应用胆碱能激动剂时的分泌中起相同作用。
