Chen Q, Cannell M, van Breemen C
Department of Molecular and Cellular Pharmacology, University of Miami School of Medicine, FL 33101.
Can J Physiol Pharmacol. 1992 Apr;70(4):509-14. doi: 10.1139/y92-066.
Force development and fura-2 fluorescence were simultaneously measured in the rabbit inferior vena cava. Discharging SR Ca2+ with either caffeine or norepinephrine prior to stimulation of Ca2+ influx induced a delay of 30-70 s between the intracellular Ca2+ signal and development of force. This delay was abolished by the application of caffeine. These data support the superficial buffer barrier hypothesis, which holds that Ca2+ entry from the extracellular space proceeds via a restricted cytoplasmic region between the inner plasmalemmal surface and the peripheral sarcoplasmic reticulum (SR). Ca2+ accumulation by this SR fraction appears to be able to delay Ca2+ entry into the deeper myoplasm where it activates the myofilaments. Caffeine and thapsigargin elevated the steady-state [Ca2+]i, suggesting a contribution by the SR Ca2+ pump to Ca2+ extrusion from the cells. Norepinephrine enhanced myofilament Ca2+ sensitivity, while caffeine decreased it.
在兔下腔静脉中同时测量了力的产生和fura-2荧光。在刺激Ca2+内流之前，用咖啡因或去甲肾上腺素释放肌浆网（SR）中的Ca2+，会在细胞内Ca2+信号和力的产生之间诱导30 - 70秒的延迟。应用咖啡因可消除这种延迟。这些数据支持表面缓冲屏障假说，该假说认为细胞外空间的Ca2+进入是通过内质膜表面和外周肌浆网（SR）之间受限的细胞质区域进行的。该SR部分的Ca2+积累似乎能够延迟Ca2+进入更深的肌浆，在那里它激活肌丝。咖啡因和毒胡萝卜素升高了稳态[Ca2+]i，表明SR Ca2+泵对细胞内Ca2+的排出有贡献。去甲肾上腺素增强了肌丝对Ca2+的敏感性，而咖啡因则降低了它。
