Shears S B, Kirk C J
Biochem J. 1984 Jun 1;220(2):417-21. doi: 10.1042/bj2200417.
Stimulation of hepatocytes with vasopressin (10 nM) in the presence of 1.25 mM extracellular Ca2+ increased glycogen phosphorylase activity 4-fold within 15s and provoked a rapid efflux of cell-associated Ca2+. Vasopressin also caused a transient increase in the Ca content of a mitochondria-rich fraction separated within seconds of hormone stimulation by a rapid fractionation technique [Shears & Kirk (1984) Biochem. J. 219, 375-382]. The Ca content of this fraction was restored to the control value within 2 min of hormone addition. These results indicate that mitochondria are not the source of the cell-associated Ca which is mobilized in the cytosol of vasopressin-stimulated hepatocytes. Rather, these organelles buffer the increase in cytosol [Ca2+] attributable to Ca mobilization from non-mitochondrial sources.
在存在1.25 mM细胞外Ca2+的情况下,用血管加压素(10 nM)刺激肝细胞,糖原磷酸化酶活性在15秒内增加了4倍,并引发了细胞相关Ca2+的快速外流。血管加压素还导致通过快速分级分离技术在激素刺激后几秒钟内分离出的富含线粒体的部分的Ca含量短暂增加[Shears & Kirk(1984年)《生物化学杂志》219,375 - 382]。在添加激素后2分钟内,该部分的Ca含量恢复到对照值。这些结果表明,线粒体不是血管加压素刺激的肝细胞胞质溶胶中动员的细胞相关Ca的来源。相反,这些细胞器缓冲了由于从非线粒体来源动员Ca而导致的胞质溶胶[Ca2+]的增加。