Karsanov N V, Khugashvili Z G
Biokhimiia. 1983 Aug;48(8):1359-64.
It was demonstrated that under normal conditions calmodulin and exogenous 3':5'-AMP-dependent protein kinase considerably active Ca2+ transport by sarcoplasmic reticulum of rabbit myocardium; a combined action of these compounds produces an additive effect. The protein-inhibitor of 3':5'-AMP-dependent protein kinase and trifluoroperazine eliminate the activating effect of 3':5'-AMP-dependent protein kinase; in addition, trifluoroperazine decreases significantly the basal level of Ca2+ uptake. The 3':5'-AMP-dependent activation of Ca2+ transport becomes apparent after Ca2+-calmodulin-dependent phosphorylation of FSR membrane proteins. In toxico-allergic myocarditis calmodulin and 3':5'-AMP-dependent protein kinase do not activate the low level of Ca2+ uptake. No differences were observed between the action of calmodulin and 3':5'-AMP-dependent protein kinase isolated from normal and pathological rabbit heart. A conclusion is drawn that the decrease of Ca2+ transport is due to the impairment of Ca2+-calmodulin and 3':5'-AMP-dependent phosphorylation in sarcoplasmic reticulum membranes.
结果表明,在正常情况下,钙调蛋白和外源性3':5'-AMP依赖性蛋白激酶可显著激活兔心肌肌浆网的Ca2+转运;这些化合物的联合作用产生相加效应。3':5'-AMP依赖性蛋白激酶的蛋白抑制剂和三氟拉嗪可消除3':5'-AMP依赖性蛋白激酶的激活作用;此外,三氟拉嗪可显著降低Ca2+摄取的基础水平。Ca2+转运的3':5'-AMP依赖性激活在FSR膜蛋白的Ca2+ -钙调蛋白依赖性磷酸化后变得明显。在中毒性变应性心肌炎中,钙调蛋白和3':5'-AMP依赖性蛋白激酶不能激活低水平的Ca2+摄取。从正常和病理兔心脏分离的钙调蛋白和3':5'-AMP依赖性蛋白激酶的作用未观察到差异。得出结论,Ca2+转运的降低是由于肌浆网膜中Ca2+ -钙调蛋白和3':5'-AMP依赖性磷酸化受损所致。