BACKGROUND Slow delayed-rectifier potassium current (IKs) channels, made of the pore-forming KCNQ1 and auxiliary KCNE1 subunits, play a key role in determining action potential duration (APD) in cardiac myocytes. The consequences of drug-induced KCNQ1 splice alteration remain unknown. OBJECTIVE To study the modulation of KCNQ1 alternative splicing by amiloride and the consequent changes in IK...

OBJECTIVE Rapid electrical activity in pulmonary veins (PVs) has been proposed as a mechanism for focal atrial fibrillation. The way in which the myocardial sleeve inside PVs can form a substrate for focal activity is not well understood. Therefore, we have studied tissue structure and connexin distribution at the veno-atrial transition in the dog. METHODS In adult mongrel dogs, the anatomy o...

Introduction: Native myocardium consists of several cell types of which 1/3 are myocytes and most of the non-myocytes are fibroblasts [1]. Cardiac myocytes are the largest cells in the myocardium, they occupy ~90% of the volume and are responsible for synchronous contractions of the ventricles. The main roles of cardiac fibroblasts are to secrete the components of the extra-cellular matrix (ECM...

To determine whether angiotensin II (Ang II) stimulation of adult ventricular myocytes in vitro results in cellular hypertrophy, the changes in myocyte volume and protein content per cell were examined by confocal microscopy. Moreover, the possibility was considered that the upregulation of Ang II receptors on myocytes after infarction may potentiate and/or accelerate Ang II-mediated myocyte gr...

Previous studies have shown that digitalis drugs, acting as specific inhibitors of cardiac Na(+)/K(+)-ATPase, not only cause positive inotropic effects, but also activate cell signaling pathways that lead to cardiac myocyte hypertrophy. A major aim of this work was to assess the role of Na(+)/Ca(2+)-exchanger, NCX1, in the above two seemingly related drug effects. Using a mouse with ventricular...

Cardiac myocytes are activated by hormonal and mechanical signals and respond in a variety of ways, from altering contractile function to inducing cardio-protection and growth responses. The use of genetic mouse models allows one to examine the role of cardiac-specific and other genes in cardiac function, hypertrophy, cardio-protection, and diseases such as ischemia and heart failure. However, ...

Vascular endothelial growth factor (VEGF) has been proposed to be among the candidate factors with the most potential to play a role in ischemia-induced collateral vessel formation. Recently, we found that VEGF activated the mitogen-activated protein kinase cascade in cultured rat cardiac myocytes. To elucidate how VEGF affects adhesive interaction of cardiac myocytes with the extracellular mat...

Senescence marker protein-30 (SMP30) decreases with aging. Mice with SMP30 deficiency, a model of aging, have a short lifespan with increased oxidant stress. To elucidate SMP30's effect on coronary circulation derived from myocytes, we measured the changes in the diameter of isolated coronary arterioles in wild-type (WT) mice exposed to supernatant collected from isolated paced cardiac myocytes...

Excessive nitric oxide (NO) production within the heart is implicated in the pathogenesis of myocyte death, but the mechanism whereby NO kills cardiac myocytes is not known. To determine whether NO may trigger programmed cell death (apoptosis) of adult rat ventricular myocytes in culture, the NO donor S-nitroso- N-acetylpenicillamine (SNAP) was shown to kill purified cardiac myocytes in a dose-...

Hypertension-induced cardiac hypertrophy alters the amplitude and time course of the systolic Ca2+ transient of subepicardial and subendocardial ventricular myocytes. The present study was designed to elucidate the mechanisms underlying these changes. Myocytes were isolated from the left ventricular subepicardium and subendocardium of 20-wk-old spontaneously hypertensive rats (SHR) and age-matc...