Galoyan A A, Kevorkian G A, Voskanian L H, Alexanian S S, Muradian M S
Institute of Biochemistry of Acad. Sci. Arm. SSR, Yerevan.
Neurochem Res. 1988 May;13(5):493-8. doi: 10.1007/BF01268886.
Neurohormone C (NC) is a glycopeptide isolated from bovine hypothalamus, which inhibits Ca-calmodulin (CaM)-dependent cAMP and cGMP phosphodiesterase (PDE) and is a regulator of Ca in the cell. Distribution of [45Ca]CaCl2 in the mitochondria and reticulum (SR) of heart and brain mitochondria and changes of Ca-binding proteins in these organelles under NC influence have been studied in the myocardium before and after isoproterenol-induced necrosis. Intraperitoneal administration of 80-100 mU of PDE inhibitory activity of NC to rats did not cause any noticeable changes in the protein content of intracellular organelles, but altered the affinity of certain proteins to 45Ca2+. This property of NC was especially noticeable after isoproterenol necrosis. Necrotic injury of the myocardium induced Ca2+ storage in the mitochondria and SR of brain, and decreased the Ca2+ concentration in myocardial mitochondria. NC injection to the animals with necrosis was followed by Ca2+ release from all the studied organelles.
神经激素C（NC）是一种从牛下丘脑分离出的糖肽，它能抑制钙 - 钙调蛋白（CaM）依赖性的环磷酸腺苷（cAMP）和环磷酸鸟苷（cGMP）磷酸二酯酶（PDE），并且是细胞内钙的调节剂。在异丙肾上腺素诱导心肌坏死前后，研究了[45Ca]氯化钙在心脏和脑线粒体的线粒体及肌浆网（SR）中的分布以及在NC影响下这些细胞器中钙结合蛋白的变化。给大鼠腹腔注射具有80 - 100 mU PDE抑制活性的NC，并未引起细胞内细胞器蛋白质含量的任何明显变化，但改变了某些蛋白质对45Ca2+的亲和力。在异丙肾上腺素诱导心肌坏死后，NC的这一特性尤为明显。心肌坏死损伤导致脑线粒体和肌浆网中Ca2+储存增加，并降低了心肌线粒体中的Ca2+浓度。给坏死动物注射NC后，所有研究的细胞器均出现Ca2+释放。
