Cardiac Hypertrophy and Altered Cellular Electrical Activity of the Myocardium

TenEick, R. E.; Houser, Steven R.; Bassett, Arthur L.

doi:10.1007/978-1-4613-0873-7_28

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%

Calcium current in single cells isolated from normal and hypertrophied rat heart. Effects of beta-adrenergic stimulation.

Scamps

Mayoux

Charlemagne

et al. 1990

Circulation Research

128

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mentioning

confidence: 74%

Calcium current in single cells isolated from normal and hypertrophied rat heart. Effects of beta-adrenergic stimulation.

Scamps

Mayoux

Charlemagne

et al. 1990

Circulation Research

128

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“…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%

Electrophysiological Characterization of Cardiac Muscarinic Acetylcholine Receptors: Different Subtypes Mediate Different Potassium Currents

Shi

Yang

Xu³

et al. 2003

Cell Physiol Biochem

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To characterize electrophysiologically the K⁺ currents mediated by various mAChR subtypes, we performed detailed whole-cell patch-clamp studies in canine atrial myocytes. I_KACh was induced by 1 mM ACh (acetylcholine) or by arecaidine but-2-ynyl ester tosylate (100 nM, an M₂ receptor selective agonist) and was blocked by methoctramine (20 nM, an M₂ receptor selective antagonist). Tetramethylammonium (0.5 mM) activated a K⁺ conductance with delayed rectifying properties (I_KM3) and the currents were highly sensitive to 4-diphenylacetoxy-N-methylpiperidine methiodide (2 nM, an M₃ receptor inhibitor). 4-aminopyridine (1 mM) induced a delayed rectifier-like current (I_K4AP) which was selectively suppressed by tropicamide (200 nM, an M₄ receptor blocker). The current waveforms, I-V relationships, steady-state voltage-dependence, kinetics and pharmacological properties of these three currents were different from one another and distinct from the classical delayed rectifier K⁺ currents (I_Kr and I_Ks). Both I_KACh and I_K4AP were sensitive to pertussis ntoxin, whereas I_KM3 was not. Isoproterenol (1 mM) markedly depressed I_KM3, but increased I_K4AP and did not alter I_KACh. The effects of isoproterenol were reversed by propranolol (1 mM); and ACh completely suppressed I_KM3 and I_K4AP. The results suggest that the K⁺ currents mediated by different subtypes of mAChR represent different populations of K⁺ channels and that the cholinergic regulation of the heart’s electrical function is a consequence of activating multiple mAChRs linked to different effector systems with potentially varying signal transduction.

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“…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.…”

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confidence: 99%

Molecular basis of transient outward K⁺ current diversity in mouse ventricular myocytes

Guo

London

et al. 1999

The Journal of Physiology

195

223

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Two kinetically and pharmacologically distinct transient outward K+ currents, referred to as Ito,f and Ito,s, have been distinguished in mouse left ventricular myocytes. Ito,f is present in all left ventricular apex cells and in most left ventricular septum cells, whereas Ito,s is identified exclusively in left ventricular septum cells. Electrophysiological recordings from ventricular myocytes isolated from animals with a targeted deletion of the Kv1.4gene (Kv1.4−/− mice) reveal that Ito,s is undetectable in cells isolated from the left ventricular septum (n= 26). Ito,f density in both apex and septum cells, in contrast, is not affected by deletion of Kv1.4. Neither the 4‐AP‐sensitive, slowly inactivating K+ current, IK,slow, nor the steady‐state non‐inactivating K+ current, ISS, is affected in Kv1.4−/− mouse left ventricular cells. In myocytes isolated from transgenic mice expressing a dominant negative Kv4.2 α subunit, Kv4.2W362F, Ito,f is eliminated in both left ventricular apex and septum cells. In addition, a slowly inactivating transient outward K+ current similar to Ito,s in wild‐type septum cells is evident in myocytes isolated from left ventricular apex of Kv4.2W362F‐expressing transgenics. The density of Ito,s in septum cells, however, is unaffected by Kv4.2W362F expression. Western blots of fractionated mouse ventricular membrane proteins reveal a significant increase in Kv1.4 protein level in Kv4.2W362F‐expressing transgenic mice. The protein levels of other Kv α subunits, Kv1.2 and Kv2.1, in contrast, are not affected by the expression of the Kv4.2W362F transgene. The results presented here demonstrate that the molecular correlates of Ito,f and Ito,s in adult mouse ventricle are distinct. Kv1.4 underlies mouse ventricular septum Ito,s, whereas Kv α subunits of the Kv4 subfamily underlie mouse ventricular apex and septum Ito,f. The appearance of the slow transient outward K+ current in Kv4.2W362F‐expressing left ventricular apex cells with properties indistinguishable from Ito,s in wild‐type cells is accompanied by an increase in Kv1.4 protein expression, suggesting that the upregulation of Kv1.4 underlies the observed electrical remodeling in Kv4.2W362F‐expressing transgenics.

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Cardiac Hypertrophy and Altered Cellular Electrical Activity of the Myocardium

Cited by 16 publications

References 100 publications

Calcium current in single cells isolated from normal and hypertrophied rat heart. Effects of beta-adrenergic stimulation.

Calcium current in single cells isolated from normal and hypertrophied rat heart. Effects of beta-adrenergic stimulation.

Electrophysiological Characterization of Cardiac Muscarinic Acetylcholine Receptors: Different Subtypes Mediate Different Potassium Currents

Molecular basis of transient outward K⁺ current diversity in mouse ventricular myocytes

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Cardiac Hypertrophy and Altered Cellular Electrical Activity of the Myocardium

Cited by 16 publications

References 100 publications

Calcium current in single cells isolated from normal and hypertrophied rat heart. Effects of beta-adrenergic stimulation.

Calcium current in single cells isolated from normal and hypertrophied rat heart. Effects of beta-adrenergic stimulation.

Electrophysiological Characterization of Cardiac Muscarinic Acetylcholine Receptors: Different Subtypes Mediate Different Potassium Currents

Molecular basis of transient outward K+ current diversity in mouse ventricular myocytes

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Molecular basis of transient outward K⁺ current diversity in mouse ventricular myocytes