cardiomegaly/kalij

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Basal and IGF-I-dependent regulation of potassium channels by MAP kinases and PI3-kinase during eccentric cardiac hypertrophy.

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The potassium channels I(K) and I(K1), responsible for the action potential repolarization and resting potential respectively, are altered during cardiac hypertrophy. The activation of insulin-like growth factor-I (IGF-I) during hypertrophy may affect channel activity. The aim was to examine the

The Mechanism of High-Output Cardiac Hypertrophy Arising From Potassium Channel Gain-of-Function in Cantú Syndrome

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Dramatic cardiomegaly arising from gain-of-function (GoF) mutations in the ATP-sensitive potassium (K_ATP) channels genes, ABCC9 and KCNJ8, is a characteristic feature of Cantú syndrome (CS). How potassium channel over-activity results in cardiac hypertrophy, as well as the

Molecular mechanisms regarding potassium bromate‑induced cardiac hypertrophy without apoptosis in H9c2 cells.

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Cardiac hypertrophy is commonly involved in cardiac injury. Oxidative stress can induce cardiac hypertrophy with apoptosis. Potassium bromate (KBrO3) has been widely used as a food additive due to its oxidizing properties. In the present study, the rat‑derived heart cell line H9c2 was used to

Arrhythmogenic β-adrenergic signaling in cardiac hypertrophy: The role of small-conductance calcium-activated potassium channels via activation of CaMKII.

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Sustained ventricular arrhythmias (SVAs) lead to sudden cardiac death, for which β- adrenoreceptor blockers are effective. We hypothesized that electrophysiological changes and arrhythmias by β- adrenoreceptor stimulation are crucially related to activation of small-conductance calcium-activated

An increased TREK-1-like potassium current in ventricular myocytes during rat cardiac hypertrophy.

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To elucidate the expression and identify the functional changes of 2 pore domain potassium channel TREK-1 during cardiac hypertrophy in rats, left ventricular hypertrophy was induced by subcutaneous injection with isoproterenol. Western blot was used to detect the expression of TREK-1 channel

Potassium channel remodeling in cardiac hypertrophy.

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Cardiac hypertrophy is an adaptive process against increased work loads; however, hypertrophy also presents substrates for lethal ventricular arrhythmias, resulting in sudden arrhythmic deaths that account for about one third of deaths in cardiac hypertrophy. To maintain physiological cardiac

Cardiac hypertrophy diminished the effects of isoproterenol on delayed rectifier potassium current in rat heart.

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We investigated the association between sympathetic nerve activity and delayed rectifier potassium current (I(K)) in hypertrophic rat hearts. Left ventricular hypertrophy was induced by a 50% constriction of suprarenal abdominal aorta for 6 weeks. The effects of isoproterenol on action potential

Mitochondrial ATP-sensitive potassium channel opening inhibits isoproterenol-induced cardiac hypertrophy by preventing oxidative damage.

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Cardiac hypertrophy is a chronic complex disease that occurs in response to hemodynamic load and is accompanied by oxidative stress and mitochondrial dysfunction. Mitochondrial ATP-sensitive K channels (mitoKATPs) have previously been shown to prevent oxidative cardiac damage under conditions of

Up-regulation of miR-195 contributes to cardiac hypertrophy-induced arrhythmia by targeting calcium and potassium channels

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Previous studies have confirmed that miR-195 expression is increased in cardiac hypertrophy, and the bioinformatics website predicted by Targetscan software shows that miR-195 can directly target CACNB1, KCNJ2 and KCND3 to regulate Cavβ1, Kir2.1 and Kv4.3 proteins expression. The purpose of this

Potassium depletion and cardiac hypertrophy: how does it work?

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The Pathophysiology of Cardiac Abnormalities in Cantu Syndrome: Perspective on "The Mechanism of High-Output Cardiac Hypertrophy Arising From Potassium Channel Gain-of-Function in Cantú Syndrome"

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Elevated blood pressure and cardiac hypertrophy after ablation of the gly96/IEX-1 gene.

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gly96/IEX 1 is a growth- and apoptosis-regulating, immediate early gene that is widely expressed in epithelial and vascular tissues. In vascular tissues, expression of the gene is induced by mechanical stretch, and overexpression of the gene prevents injury-induced vascular smooth muscle hypertrophy

Temporal alterations and cellular mechanisms of transmural repolarization during progression of mouse cardiac hypertrophy and failure.

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OBJECTIVE The remodelling of transmural dispersion of repolarization (TDR) in human heart failure (HF) and in different animal models of cardiac hypertrophy or HF remains a controversial topic. We hypothesize that TDR may exhibit temporal alterations, depending on the stage of the

Angiotensin AT1 receptor-mediated attenuation of cardiac hypertrophy due to volume overload: involvement of endothelin.

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The role of angiotensin II via the angiotensin type 1 (AT1) receptor in the development of volume overload cardiac hypertrophy was investigated in adult male Wistar rats with aortic insufficiency. We examined the effects of specific angiotensin AT1 receptor blockade with losartan

[Heart hypertrophy and heart failure--experimental findings for arrhythmogenesis].

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One major cause of sudden cardiac death in heart failure is the occurrence of life-threatening polymorphic ventricular tachycardia. Especially in the early stages of heart failure half of the deaths are sudden and unexpected. The majority of these are caused by ventricular tachyarrhythmias. Whereas

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