摘要
目的:研究前胡丙素(PraC)的心脏负性肌力作用的机制.方法:使用Ca2+敏感的荧光指示剂Fura2AM,在培养的新生鼠心肌细胞测定细胞内Ca2+的瞬间变化.结果:PraC10、30μmol·L-1引起[Ca2+]i瞬间变化最大值明显减少.PraC10,30μmol·L-1能部分抑制CaCl248mmol·L-1及Bayk8644100nmol·L-1增加的[Ca2+]i瞬间变化的峰值,但对[Ca2+]i瞬间变化的基线水平没有明显的影响.Ryanodine3μmol·L-1使[Ca2+]i瞬间变化的幅度明显降低,在此基础上,PraC30μmol·L-1继续抑制[Ca2+]i的瞬间变化.结论:PraC在完整心肌的负性肌力作用可能与其部分抑制兴奋收缩偶联过程中的Ca2+内流有关.
AIMS: To study the effects of praeruptorin C (Pra-C) on [Ca2+](i) transients in cultured neonatal myocardiocytes. METHOD: Using Ca2+-sensitive fluorescent indicator, Fura 2-AM, spontaneous cytosolic Ca2+ transients were measured in cultured myocardial cells of neonatal rats. RESULTS: Pra-C 10, 30 mu mol . L(-1) caused a decrease in the peak of Ca2+ transients. Pra-C 30 mu mol . L(-1) and 10 - 30 mu mol . L(-1) inhibited partly the stimulatory effects of CaCl2 4.8 mmol . L(-1) and Bay k 8644 100 nmol . L(-1) on peak Ca2+ transients, respectively. Pra-C did not cause any marked change in the basal [Ca2+](i) level between beats. Pra-C inhibited the reduced [Ca2+](i) transients after inhibition of sarcoplasmic reticulum Ca2+ release in ryanodine pretreated cells. CONCLUSIONS: Pra-C inferred with the Ca2+ influx responsible for excitation-contraction coupling in myocardiocytes.
出处
《中国药理学报》
CSCD
1997年第1期81-84,共4页
Acta Pharmacologica Sinica
关键词
前胡丙素
心肌细胞
钙
细胞培养
coumarins
cultured cells
myocardium
calcium
Fura-2
Bay k 8644
ryanodine