高钾对大鼠脾脏中一种新型电压门控Ca2+通道的激活作用。

Activation by high potassium of a novel voltage-operated Ca2+ channel in rat spleen.

作者信息

Ko F N, Huang S Y, Teng C M

机构信息

Pharmacological Institute, College of Medicine, National Taiwan University, Taipei.

出版信息

Br J Pharmacol. 1997 Feb;120(4):565-70. doi: 10.1038/sj.bjp.0700935.

DOI:10.1038/sj.bjp.0700935

PMID:9051291

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1564497/

Abstract

High potassium produced a concentration-dependent contraction in rat isolated spleen. 2. The high potassium-induced contraction of rat spleen was abolished in Ca(2+)-free Krebs solution containing 1 mM EGTA, and the subsequent addition of 3 mM Ca2+ restored the high potassium-induced contraction to the control level. 3. Nifedipine, verapamil, diltiazem, Cd2+, Ni2+, Co2+, R-(+)-Bay K 8644 and pimozide inhibited and relaxed high potassium-induced contraction of rat spleen with IC50 and EC50 values much higher than those values in rat aorta. 4. In addition, high potassium-stimulated contraction of rat spleen was insensitive to omega-conotoxin GVIA, omega-conotoxin MVIIC and omega-agatoxin IVA. 5. The high potassium-induced contraction of rat spleen was also unaffected by tetrodotoxin (TTX), prazosin, chloroethylclonidine (CEC), yohimbine, propranolol, atropine, diphenhydramine, cimetidine, ketanserin, 3-tropanyl-indole-3-carboxylate, saralasin, indomethacin, nordihydroguaiaretic acid, GR32191B, domperidone, naloxone, chlorpromazine, suramin, (+/-)-2-amino-5-phosphonopentanoic acid, 6,7-dinitroquinoxaline-2,3-dione (DNQX), L-659,877, L-703,606, lorglumide, PD 135,158 N-methyl-D-glucamine, benextramine, amiloride, dantrolene, TMB-8, econazole, staurosporine and neomycin. 6. Forskolin and sodium nitroprusside relaxed high potassium-induced contraction of rat spleen with EC50 values of 0.55 +/- 0.04 and 20.0 +/- 2.7 microM, respectively. 7. It is concluded that high potassium may activate a novel, pharmacologically uncharacterized voltage-operated Ca2+ channel in rat spleen.

摘要

高钾可使大鼠离体脾脏产生浓度依赖性收缩。2. 在含1 mM乙二醇双（2-氨基乙基醚）四乙酸（EGTA）的无钙Krebs溶液中，高钾诱导的大鼠脾脏收缩被消除，随后加入3 mM钙离子可使高钾诱导的收缩恢复至对照水平。3. 硝苯地平、维拉帕米、地尔硫䓬、镉离子、镍离子、钴离子、R-(+)-Bay K 8644和匹莫齐特抑制并舒张高钾诱导的大鼠脾脏收缩，其半数抑制浓度（IC50）和半数有效浓度（EC50）值远高于大鼠主动脉中的相应值。4. 此外，高钾刺激的大鼠脾脏收缩对ω-芋螺毒素GVIA、ω-芋螺毒素MVIIC和ω-阿加毒素IVA不敏感。5. 高钾诱导的大鼠脾脏收缩也不受河豚毒素（TTX）、哌唑嗪、氯乙可乐定（CEC）、育亨宾、普萘洛尔、阿托品、苯海拉明、西咪替丁、酮色林、3-托烷吲哚-3-羧酸、沙拉新、吲哚美辛、去甲二氢愈创木酸、GR32191B、多潘立酮、纳洛酮、氯丙嗪、苏拉明、(±)-2-氨基-5-膦酰基戊酸、6,7-二硝基喹喔啉-2,3-二酮（DNQX）、L-659,877、L-703,606、洛谷胺、PD 135,158、N-甲基-D-葡糖胺、苯苄胺、氨氯吡咪、丹曲林、TMB-8、益康唑、星形孢菌素和新霉素的影响。6. 福斯高林和硝普钠舒张高钾诱导的大鼠脾脏收缩，其EC50值分别为0.55±0.04和20.0±2.7微摩尔。7. 得出的结论是，高钾可能激活大鼠脾脏中一种新型的、药理学特性未明确的电压门控钙离子通道。