Wang H X, Rao M R, Wang J X, Yang S J
Department of Cardiovascular Pharmacology, Nanjing Medical University, China.
Zhongguo Yao Li Xue Bao. 1997 Jan;18(1):81-4.
To study the effects of praeruptorin C (Pra-C) on [Ca2+]i transients in cultured neonatal myocardiocytes.
Using Ca(2+)-sensitive fluorescent indicator, Fura 2-AM, spontaneous cytosolic Ca2+ transients were measured in cultured myocardial cells of neonatal rats.
Pra-C 10, 30 mumol.L-1 caused a decrease in the peak of Ca2+ transients. Pra-C 30 mumol.L-1 and 10-30 mumol.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.
Pra-C inferred with the Ca2+ influx responsible for excitation-contraction coupling in myocardiocytes.
研究前胡丙素(Pra-C)对培养的新生心肌细胞内钙离子浓度([Ca2+]i)瞬变的影响。
采用钙离子敏感荧光指示剂Fura 2-AM,检测新生大鼠培养心肌细胞中的自发胞质钙离子瞬变。
10、30 μmol·L-1的Pra-C可使钙离子瞬变峰值降低。30 μmol·L-1的Pra-C以及10 - 30 μmol·L-1的Pra-C分别部分抑制了4.8 mmol·L-1氯化钙和100 nmol·L-1 Bay k 8644对钙离子瞬变峰值的刺激作用。Pra-C未引起搏动间期基础[Ca2+]i水平的明显变化。在经Ryanodine预处理的细胞中,抑制肌浆网钙离子释放后,Pra-C可抑制降低的[Ca2+]i瞬变。
Pra-C干扰了心肌细胞中负责兴奋-收缩偶联的钙离子内流。