1989
DOI: 10.1007/978-1-4613-0873-7_28
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Cardiac Hypertrophy and Altered Cellular Electrical Activity of the Myocardium

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Cited by 16 publications
(3 citation statements)
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“…[2][3][4] This has also been shown in myocytes isolated from hypertrophied hearts.5-7 Some experiments with multicellular preparations have attributed this prolongation to a slower inactivation of the slow inward current. 28 This was reinforced by the the slow component of calcium current (lCa) inactivation is increased.6'9 Besides changes in kinetics, the amplitude of the ionic currents underlying action potential could also be affected.…”
mentioning
confidence: 74%
“…[2][3][4] This has also been shown in myocytes isolated from hypertrophied hearts.5-7 Some experiments with multicellular preparations have attributed this prolongation to a slower inactivation of the slow inward current. 28 This was reinforced by the the slow component of calcium current (lCa) inactivation is increased.6'9 Besides changes in kinetics, the amplitude of the ionic currents underlying action potential could also be affected.…”
mentioning
confidence: 74%
“…This diversity has physiological implications in the heart, since different types of K + currents subserve different roles in regulating the membrane potentials and the rate of membrane repolarization [1][2][10][11]. Alterations of cardiac K + channel function and density can have profound pathophysiological consequences in a variety of myocardial diseases, including myocardial ischemia, cardiac hypertrophy, heart failure and lifethreatening arrhythmias [12][13][14]. Moreover, cardiac K + currents are also primary targets for many drugs that alter cardiac function to produce beneficial effects or to cause cardiotoxicity.…”
Section: Introductionmentioning
confidence: 99%
“…These are broad classifications, however, and it is now clear that there are multiple components of I K , and that the densities, properties and functional roles of I to and I K vary in cardiac cells isolated from different species, as well as in cells from different regions of the heart in the same species (Anumonwo et al 1991; Antzelevitch et al 1995; Barry & Nerbonne, 1996). There are also marked changes in the densities and the properties of voltage‐gated K + currents in the heart during normal development (Wetzel & Klitzner, 1996; Nerbonne, 1998) and in various myocardial disease states (Ten Eick et al 1989; Boyden & Jeck, 1995; Näbauer & Kaab, 1998). For all of these reasons, there is considerable interest in defining the properties and the molecular correlates of cardiac I to and I K channels, and in delineating the molecular mechanisms regulating the functional expression of these channels.…”
mentioning
confidence: 99%