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- W110341738 abstract "The mechanisms of action of drugs that act on myocardial contractility through different signal transduction pathways have lately been elucidated to a great extent, in particular since the introduction of novel methods for detecting changes in the intracellular concentration of Ca++ ions, ([Ca++] i), by the application of aequorin, quin-2, fura-2 and indo-1 in intact, contracting myocardial cells. It has been elucidated unequivocally that the regulation of myocardial contractility induced by cardiotonic agents is achieved either by increasing the mobilization of intracellular Ca++ ions via divergent subcellular mechanisms, by modulation of the responsiveness of myofibrils to Ca++ ions or by a combination of these two mechanisms. The mechanisms of action of drugs on myocardial contractility are classified into three processes (1). First, the binding of Ca++ ions to troponin C plays a central role by triggering a series of biochemical and mechanical processes in myofibrils which lead to sliding of myofilaments or force development, a process which is termed the central mechanism. Some drugs, such as caffeine (2) or agonists for β-adrenoceptors (3) act on the central mechanism, i.e., by respectively increasing or decreasing the affinity for troponin C to bind Ca++ ions. Second, the regulation of mobilization of intracellular Ca++ ions is a process upstream to the central mechanism and is termed the upstream mechanism. The upstream mechanism is the main process that is influenced by a number of known inotropic agents, including cardiac glycosides, catecholamines, Ca++ agonists and Ca++ antagonists." @default.
- W110341738 created "2016-06-24" @default.
- W110341738 creator A5021629429 @default.
- W110341738 date "1995-01-01" @default.
- W110341738 modified "2023-09-27" @default.
- W110341738 title "Calcium Signaling and Pharmacology of Cardiotonic Agents" @default.
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- W110341738 doi "https://doi.org/10.1007/978-1-4615-2021-4_14" @default.
- W110341738 hasPublicationYear "1995" @default.
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