摘要
在大鼠主动脉平滑肌标本上,0.5μmol.L-1硝苯吡啶能完全阻断由100mmol·L-1KCl引起的血管收缩和45Ca内流;并部分抑制苯肾上腺素引起的血管收缩效应和45Ca内流;6mmol·L-1普鲁卡因能完全阻断无钙Krebs液中苯肾上腺素引起的血管收缩和45Ca外溢,且部分阻断正常Krebs液中苯肾上腺素引起的血管收缩和45Ca内流;0.5μmol·L-1硝苯吡啶和6mmol·L-1普鲁卡因合用能阻断苯肾上腺素引起的Ca2+内流。提示:α1受体兴奋后引起的细胞外Ca2+内流可分为硝苯吡啶敏感和不敏感两部分,而后者受细胞内Ca2+释放调节。
In rat aorta, 0.5μmol. L-1nifedipine(Nif) completely blocked the contractile response and 45Ca influx induced by 100mmol. L-1 KCl and partially inhibited phenylephrine(PHE) -induced contractile response and 45Ca influx. 6 mmol. L-1 procaine competely blocked the contractile response and 45Ca efflux in Ca2+ free Krebs solution and partially inhibited contractile response and 45Ca influx in normal krebs solution induced by PHE. 0.5μmol. L-1 Nif plus 6 mmol. L-1 procaine completely blocked PHE-induced Ca2+ entry. These results suggest that the extracellular Ca2+ entry induced by activation of α1-adrenoceptor contains two components, sensitive to Nif and insensitive to Nif; The latter is partially regulated by intracel lular Ca2+ release.
出处
《中国药理学通报》
CAS
CSCD
北大核心
1994年第2期101-104,共4页
Chinese Pharmacological Bulletin
关键词
肾上腺素能
受体
血管平滑肌
钙
Ca ̄(2+) influx
Ca ̄(2+) release
α_1- adrenoceptor
smooth muslce(vascular )