Unique atrial myocyte Ca 2+ signaling

Abstract

The transient elevation of intracellular Ca2+ ([Ca2+]i) with each heartbeat underlies the activation of contraction and contributes to diverse regulatory features of cellular and subcellular behavior. Clear differences in the details of Ca2+ signaling occur in different cardiac tissues and vary in the same tissue from species to species. For example, Ca2+ sparks, the elementary unit of Ca2+ signaling in heart myocytes [1, 2] are plentiful during quiescent (diastolic) periods in ventricular myocytes from small rodents (e.g. rats and mice) but are rare in rabbits, dogs and humans. There are also important structural and cellular signaling differences in ventricular versus atrial myocytes. We now draw attention to the findings reported in this issue of the Journal of Molecular and Cellular Cardiology by Walden et al. (2009) who have examined the differences in Ca2+ signaling and in the levels of sarcoplasmic reticulum (SR) Ca2+ cycling proteins in atrial and ventricular myocytes [3]. They report the unexpected finding in rat heart that while the [Ca2+]i transient in atrial myocytes is much smaller than in ventricular myocytes, the Ca2+ uptake mechanism is more robust and abundant and the SR Ca2+ content is greater. This may be due to the higher level of expression of sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a) in atrial myocytes. This finding is surprising because the higher SR Ca2+ content might be expected to lead to Ca2+ overload. While such SR Ca2+ overload would promote arrhythmogenesis in ventricular myocytes, this is not a prominent feature of healthy atrial tissue. Here we discuss these findings and put them in context with normal and diseased atrial Ca2+ signaling.