Vaca L, Kunze D L
Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030.
Am J Physiol. 1993 Apr;264(4 Pt 2):H1319-22. doi: 10.1152/ajpheart.1993.264.4.H1319.
An agonist-induced Ca2+ influx pathway in vascular endothelium and other nonexcitable cells is closely aligned with the depletion of microsomal Ca2+ stores. The mechanism by which this occurs is unknown. In these studies 2',5',-di(tert-butyl-1,4-benzohydroquinone, a specific inhibitor of the microsomal Ca(2+)-adenosinetriphosphatase, and patch-clamp recordings were used to evaluate the relationship of inward Ca2+ current to the depletion of intracellular Ca2+ stores. The results demonstrate that depletion and refilling of Ca2+ stores control the amplitude of an electrogenic influx pathway in vascular endothelium. Prominent fluctuations in Ca2+ current occur when there is an imbalance between depletion and refilling of the stores. Furthermore, the studies suggest that the Ca2+ influx pathway is spatially in close association with the intracellular store.
血管内皮细胞和其他非兴奋性细胞中,激动剂诱导的Ca2+内流途径与微粒体Ca2+储存的耗竭密切相关。其发生机制尚不清楚。在这些研究中,使用微粒体Ca(2+)-三磷酸腺苷酶的特异性抑制剂2',5',-二(叔丁基)-1,4-苯二酚,以及膜片钳记录来评估内向Ca2+电流与细胞内Ca2+储存耗竭之间的关系。结果表明,Ca2+储存的耗竭和再充盈控制着血管内皮细胞中一个电源性内流途径的幅度。当储存的耗竭和再充盈之间存在不平衡时,Ca2+电流会出现显著波动。此外,研究表明Ca2+内流途径在空间上与细胞内储存密切相关。