The cardiac ryanodine receptor, but not sarcoplasmic reticulum Ca²⁺-ATPase, is a major determinant of Ca²⁺ alternans in intact mouse hearts.

ABSTRACT: Sarcoplasmic reticulum (SR) Ca²⁺ cycling is governed by the cardiac ryanodine receptor (RyR2) and SR Ca²⁺-ATPase (SERCA2a). Abnormal SR Ca²⁺ cycling is thought to be the primary cause of Ca²⁺ alternans that can elicit ventricular arrhythmias and sudden cardiac arrest. Although alterations in either RyR2 or SERCA2a function are expected to affect SR Ca²⁺ cycling, whether and to what extent altered RyR2 or SERCA2a function affects Ca²⁺ alternans is unclear. Here, we employed a gain-of-function RyR2 variant (R4496C) and the phospholamban-knockout (PLB-KO) mouse model to assess the effect of genetically enhanced RyR2 or SERCA2a function on Ca²⁺ alternans. Confocal Ca²⁺ imaging revealed that RyR2-R4496C shor

SUBMITTER: Sun B 

PROVIDER: S-EPMC6120204 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature