Protein kinase C-mediated calcium signaling as the basis for cardiomyocyte plasticity.

Protein kinase C is the superfamily of intracellular effector molecules which control crucial cellular functions. Here, we for the first time did the percentage estimation of all known PKC and PKC-related isozymes at the individual cadiomyocyte level. Broad spectrum of PKC transcripts is expressed in the left ventricular myocytes.

Cardiomyocytes generating spontaneous Ca-transients as tools for precise estimation of sarcoplasmic reticulum Ca transport.

Spontaneous Ca-transient (wave) generation in isolated cardiomyocytes is well established phenomenon which poses a lot of questions about myocardial excitability. Current studies of spontaneous Ca-activity in cardiac cells mainly relate to the kinetic characteristics, classification and simulation of Ca-events through ryanodine receptor (RyR) activity modeling. Here, for the first time we pay attention to the Ca-transients having stationary kinetics for correct estimation of the sarcoplasmic reticulum Ca transport.

Upregulation of α2-adrenoceptor synthesis in SHR cardiomyocytes: Recompense without sense - Increased amounts, impaired commands.

Aims: to investigate α2-AR subtype distribution and the relationship between receptor amounts and their functionality in normotensive and spontaneously hypertensive rats.

Methods: experiments were performed on left ventricular cardiomyocytes isolated from Wistar rats and SHR (2-2.5 months).

Disturbance of I-imidazoline receptor signal transduction in cardiomyocytes of Spontaneously Hypertensive Rats.

Imidazoline receptor of the first type (IR) in addition to the established inhibition of sympathetic neurons may mediate the direct control of myocellular functions. Earlier, we revealed that I-mediated signaling in the normotensive rat cardiomyocytes suppresses the nitric oxide production by endothelial NO synthase, impairs sarco(endo)plasmic reticulum Ca-ATPase (SERCA) activity, and elevates intracellular calcium in the cytosol. Also, I-agonists counteract β-adrenoceptor stimulation effects in respect to voltage-gated calcium currents.

Analysis of the modal hypothesis of Ca2+-dependent inactivation of L-type Ca2+ channels.

A kinetic model of Ca2+-dependent inactivation (CDI) of L-type Ca2+ channels was developed. The model is based on the hypothesis that postulates the existence of four short-lived modes with lifetimes of a few hundreds of milliseconds. Our findings suggest that the transitions between the modes is primarily determined by the binding of Ca2+ to two intracellular allosteric sites located in different motifs of the CI region, which have greatly differing binding rates for Ca2+ (different k(on)).