Sarcoplasmic reticulum Ca2+ regulatory protein gene expression in human right atrium under hemodynamic overload

Sarcoplasmic reticulum (SR) Ca2+ adenosine triphosphatase (ATPase) mRNA exp ression is reduced in the failing human myocardium. However, it is not know n whether SR Ca2+-regulatory protein gene expression is altered in human my ocardial tissue subjected to pressure overload or volume overload. We sough t to determine whether SR Ca2+-regulatory protein gene expression is altere d in human atrial tissue subjected to mechanical overload. We obtained righ t atrial myocardial tissue (about 250 mg) at open-heart surgery from three groups of patients: no hemodynamic overload to the right atrium (control gr oup; 12 patients), atrial septal defect (ASD group; 8 patients), and tricus pid regurgitation (TR group; 7 patients). We measured the myocyte size, the area of interstitial fibrosis, SR Ca2+-ATPase, and ryanodine receptor mRNA abundance. The isolated cardiocyte area and the percent area of interstiti al fibrosis were in the order TR > ASD > control (P < 0.05). The SR Ca2+-AT Pase mRNA level in TR was significantly decreased (P = 0.004) compared with the control, whereas in the ASD group it did not differ significantly from control. There were no significant differences in ryanodine receptor mRNA levels among the three groups. SR Ca2+-ATPase gene expression was downregul ated in human atrial tissue with TR but not in ASD, which might have result ed from the differences in the degree and/or the type of hemodynamic overlo ad to the myocardium.