Stimulation of ICa by basal PKA activity is facilitated by caveolin-3 in cardiac ventricular myocytes.

L-type Ca channels (LTCC), which play a key role in cardiac excitation-contraction coupling, are located predominantly at the transverse (t-) tubules in ventricular myocytes. Caveolae and the protein caveolin-3 (Cav-3) are also present at the t-tubules and have been implicated in localizing a number of signaling molecules, including protein kinase A (PKA) and β2-adrenoceptors. The present study investigated whether disruption of Cav-3 binding to its endogenous binding partners influenced LTCC activity.

Ca efflux via the sarcolemmal Ca ATPase occurs only in the t-tubules of rat ventricular myocytes.

The transverse (t-) tubule network is an important site for Ca influx and release during excitation-contraction coupling in cardiac ventricular myocytes; however, its role in Ca extrusion is less clear. The present study was designed to investigate the relative contributions of Ca extrusion pathways across the t-tubule and surface membranes. Ventricular myocytes were isolated from the hearts of adult male Wistar rats and detubulated using formamide.

Localised Ca channel phosphorylation modulates the distribution of L-type Ca current in cardiac myocytes.

The t-tubule network is central to excitation-contraction coupling in mammalian cardiac ventricular myocytes, with recent studies showing that the majority of Ca influx via the L-type Ca current (I(Ca)) occurs across the t-tubule membrane. The present study investigated whether tonic phosphorylation of the L-type Ca channel is different at the t-tubule and surface membranes, and if this could account for the high density of I(Ca) at the t-tubules. Ventricular myocytes were isolated from male Wistar rats and detubulated using formamide.

Coronary artery disease progression is associated with increased resistance of hearts and myocytes to cardiac insults.

Objective: To investigate whether coronary artery disease alters vulnerability of hearts and myocytes to cardiac insults. To address this issue, we developed an experimental model of coronary artery disease.

Design: Prospective, experimental study.