Altered signal transduction in cardiac ventricle overexpressing A(1)-adenosine receptors.

Objective: The aim of the present study was to assess the effects of A(1)-adenosine receptor (A1-AR) stimulation in ventricle of A(1)-adenosine receptor overexpressing mice (transgenic mice, TG).

Methods: Effects of the A(1)-adenosine receptor agonist R-PIA ((-)-N(6)-phenylisopropyladenosine) on phosphorylation of phospholamban (PLB), Ca(2+) transients, Ca(2+) currents and cell shortening were studied in isolated ventricular cardiomyocytes.

Results: R-PIA alone did not affect contractility in isolated electrically stimulated cardiomyocytes from wild-type mice (WT) or TG.

Junctional sarcoplasmic reticulum transmembrane proteins in the heart.

The uptake of calcium into the sarcoplasmic reticulum (SR) and its subsequent release from the SR play a key role in the regulation of the cytosolic calcium concentration and the excitation-contraction coupling in cardiac muscle. While calcium uptake, catalyzed by the calcium-dependent ATPase, is thought to occur throughout the SR, the release of calcium is controlled by a complex of proteins localized to a distinct region, the junctional SR. This complex consists of the calcium release channel or ryanodine receptor (RyR), the high capacity calcium-binding protein calsequestrin located in the lumen of the junctional SR, and the junctional SR transmembrane proteins triadin 1 and junctin which are hypothesized to anchor calsequestrin to the RyR.