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• W2168694728 abstract "Arterial smooth muscle (ASM) contraction is triggered by agonist-evoked Ca2+ mobilization from sarcoplasmic reticulum (SR). The amount of Ca2+ released, and thus, the magnitude of the contractions, depends directly on SR Ca2+ content. Na+ pump inhibition by cardiotonic steroids (CTS) indirectly increases the Ca2+ content of the SR and, thus, contractility. This sequence of events does not, however, account for the multiple Na+ pump alpha subunit isoforms with different affinities for Na+ and for CTS, nor does it explain the cardiotonic and vasotonic effects of low doses of CTS that do not elevate cytosolic Na+ or Ca2+. We show that the Na+ pump high ouabain affinity (alpha3) isoform and the plasmalemmal (PM) Na/Ca exchanger are confined to PM domains that overlie junctional SR in ASM, while low ouabain affinity alpha1 and the PM Ca2+ pump are uniformly distributed in the PM. Thus, low doses of CTS, including an endogenous ouabain-like compound, influence cytosolic Na+ and (indirectly) Ca2+ concentrations only in the cytoplasmic clefts between the PM and junctional SR (a functional unit we call the plasmerosome). In turn, this modulates the Ca2+ content of the junctional SR and cell responsiveness." @default.
• W2168694728 created "2016-06-24" @default.
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• W2168694728 date "1998-01-01" @default.
• W2168694728 modified "2023-09-26" @default.
• W2168694728 title "The Cellular Mechanism of Action of Cardiotonic Steroids: A New Hypothesis" @default.
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• W2168694728 doi "https://doi.org/10.3109/10641969809053247" @default.
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