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Cardiac c-kit+ progenitor cells are important for maintaining cardiac homeostasis and can potentially contribute to myocardial repair. However, cellular physiology of human cardiac c-kit+ progenitor cells is not well understood. The present study investigates the functional store-operated Ca2+ entry (SOCE) channels and the potential role in regulating cell cycling and migration using confocal microscopy, RT-PCR, Western blot, coimmunoprecipitation, cell proliferation, and migration assays. We found that SOCE channels mediated Ca2+ influx, and TRPC1, STIM1, and Orai1 were involved in the formation of SOCE channels in human cardiac c-kit+ progenitor cells. Silencing TRPC1, STIM1, or Orai1 with the corresponding siRNA significantly reduced the Ca2+ signaling through SOCE channels, decreased cell proliferation and migration, and reduced expression of cyclin D1, cyclin E, and/or p-Akt. Our results demonstrate the novel information that Ca2+ signaling through SOCE channels regulates cell cycling and migration via activating cyclin D1, cyclin E, and/or p-Akt in human cardiac c-kit+ cells. [ABSTRACT FROM AUTHOR]

Adrenomedullin (ADM) is upregulated in cardiac tissue under various pathophysiological conditions, particularly in septic shock. The intra-cellular mechanisms involved in the effect of ADM on adult rat ventricular myocytes are still to be elucidated. Ventricular myocytes were isolated from adult rats 4 h after an intraperitoneal injection of lipopolysaccharide (LPS, 10 mg/kg). Membrane potential and L-type calcium current (ICa,L) were determined using whole cell patch-clamp methods. APD in LPS group was significantly shorter than control values (time to 50% repolarization: LPS, 169 ± 2 ms; control, 257 ± 2 ms, P < 0.05; time to 90% repolarization: LPS, 220 ± 2 ms; control, 305 ± 2 ms, P < 0.05). ICa,L density was significantly reduced in myocytes from the LPS group (-3.2 ± 0.8 pA/pF) compared with that of control myocytes (-6.7 ± 0.3 pA/pF, P < 0.05). The ADM antagonist ADM-(22-52) reversed the shortened APD and abolished the reduction of ICa,L in shock myocytes. In myocytes from control rats, incubating with ADM for 1 h induced a marked decrease in peak ICa,L density. This effect was reversed by ADM-(22-52). The Gi protein inhibitor, pertussis toxin (PTX), the protein kinase A (PKA) inhibitor, KT-5720, and the specific cyclo-oxygenase 2 (COX-2) inhibitor, nimesulide, reversed the LPS-induced reduction in peak ICa,L. The results suggest a COX-2-involved PKA-dependent switch from G, coupled to PTX-sensitive Gi coupling by ADM in adult rat ventricular myocytes. The present study delineates the intracellular pathways involved in ADM-mediated effects on ICa,L in adult rat ventricular myocytes and also suggests a role of ADM in sepsis. [ABSTRACT FROM AUTHOR]

Investigates the transmural action potential (AP) and ionic current remodeling in ventricles of failing canine hearts. Remodeling of heterogeneous AP in ventricular cells of heart failure (HF); Early afterdepolarizations (EAD) in cells from failing hearts; Comparison with previous findings of ionic current remodeling in HF.

Presents information on a study which examined the effects of osmotic swelling on the components of excitation-contraction coupling in ventricular myocytes. Methodology; Results and discussion.

Presents information on a study which examined whether block of cardiac sodium channels by gadolinium might contribute to its antiarrhythmic efficacy on stretch-induced ectopic activity. Materials and methods; Results; Discussion.

Deals with a study which identified a novel transient outward potassium current that exhibits inward-going rectification in guinea pig atrial and ventricular myocytes. Description of the transient outward current; Effect of aminopyridine on transient outward current; Current-voltage relationship of the inward-going rectification; Kinetics of the inward-going rectification.

Presents information on a study which determined whether adenosine activation of potassium channels in excised membrane patches is mediated by protein kinase C (PKC). Methodology; Results and discussion.

Presents information on a study which determined the relation between rate-dependent changes in action potential duration and changes in calcium ion in human ventricular myocytes. Methodology; Results and discussion.

Evaluates the heterogeneity of cardiac action potential (AP), transient potassium efflux current and influx current of potassium in the right ventricle of the human heart. Details on cardiac electrophysiology; Methodology of the study; Results of the study.

Discusses the electric properties of intracellular calcium current (ICa) at physiological temperatures in human atriums. Peak and mean maximum current density of ICa upon depolarization of human atrial myocytes at 36 degrees Celsius; Description of frequency dependence of ICa; Compatibility of ICa role to the overlap between activation and inactivation curves.