Modification of the function of cardiac subcellular organelles by insulin.

Advances in myocardiology Pub Date : 1985-01-01
G N Pierce, P K Ganguly, A Dzurba, N S Dhalla
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Abstract

Although insulin is known to elicit a positive inotropic effect in cardiac-muscle preparations, little is known concerning the mechanism responsible for this action. Because various subcellular organelles such as mitochondria, sarcoplasmic reticulum (SR), sarcolemma, and myofibrils are intimately involved in determining the cardiac contractile function, the effects of insulin (0.1-1000 mU/ml) on some selected enzymatic activities associated with these organelles were investigated. Insulin significantly enhanced Ca2+ uptake and Ca2+-stimulated ATPase activities of SR preparations obtained by two different methods. Insulin had no effect on mitochondrial Ca2+ uptake and ATPase activities or myofibrillar ATPase activities. Sarcolemmal Na+, K+-ATPase activity was stimulated only in the presence of 1 U/ml insulin, whereas sarcolemmal Ca2+ pump activity was increased by all insulin concentrations employed. Sarcolemmal Ca2+-ATPase activity and ATP-independent Ca2+ binding were augmented in the presence of 1 U/ml insulin only. These subcellular effects of insulin, either alone or in concert, may partially explain the positive inotropic action of insulin.

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胰岛素对心脏亚细胞细胞器功能的影响。
虽然已知胰岛素在心肌制剂中引起积极的肌力作用,但对这种作用的机制知之甚少。由于线粒体、肌浆网(SR)、肌膜和肌原纤维等多种亚细胞细胞器与心脏收缩功能密切相关,因此研究了胰岛素(0.1-1000 mU/ml)对与这些细胞器相关的一些选定酶活性的影响。胰岛素显著提高Ca2+摄取和Ca2+刺激的atp酶活性通过两种不同的方法获得的SR制剂。胰岛素对线粒体Ca2+摄取和atp酶活性或肌纤维atp酶活性没有影响。只有在1 U/ml胰岛素的存在下,肌上皮Na+, K+- atp酶活性才会受到刺激,而肌上皮Ca2+泵活性则会在所有胰岛素浓度下增加。仅在1 U/ml胰岛素存在时,肌上皮Ca2+- atp酶活性和atp独立的Ca2+结合增强。胰岛素的这些亚细胞作用,无论是单独的还是协同的,可能部分解释了胰岛素的正性肌力作用。
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Influence of Na/K pump current on action potentials in Purkinje fibers. The effects of intracellular Na on contraction and intracellular pH in mammalian cardiac muscle. Molecular approach to the calcium channel. The measurement of cardiac membrane channels following their incorporation into phospholipid bilayers. Calmodulin in the regulation of calcium fluxes in cardiac sarcolemma.
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