Plasma membrane Ca2+ ATPase 1 is required for maintaining atrial Ca2+ homeostasis and electrophysiological stability in the mouse

Abstract

To determine the role of PMCA1 in maintaining Ca²⁺ homeostasis and electrical stability in the atrium under physiological and stress conditions, mice with a cardiomyocyte-specific deletion of PMCA1 (PMCA1^cko) and their control littermates (PMCA1^loxP/loxP) were studied at the organ and cellular levels.   At the organ level, the PMCA1^cko hearts became more susceptible to atrial arrhythmias under rapid programmed electrical stimulation (PES) compared with the PMCA1^loxP/loxP hearts, and such arrhythmic events became more severe under Ca²⁺ overload conditions. At the cellular level, the occurrence of irregular-type APs of PMCA1^cko atrial myocytes increased significantly under Ca²⁺ overload conditions and/or at higher frequency of stimulation. The decay of Na⁺-Ca²⁺ exchanger (NCX) current that followed a stimulation protocol was significantly prolonged in PMCA1^cko atrial myocytes under basal conditions, with Ca²⁺ overload leading to even greater prolongation. In conclusion, PMCA1 is required for maintaining Ca²⁺ homeostasis and electrical stability in the atrium. This is particularly critical during fast removal of Ca²⁺ from the cytosol which is required under stress conditions.

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