Maximal acceleration of Ca2+ release refractoriness by β-adrenergic stimulation requires dual activation of kinases PKA and CaMKII in mouse ventricular myocytes
Abstract
Refractoriness of calcium release in heart cells is altered in several disease states, but the physiological mechanisms that regulate this process are incompletely understood. We examined refractoriness of calcium release in mouse ventricular myocytes and investigated how activation of different intracellular signalling pathways influenced this process. We found that refractoriness of calcium release is abbreviated by stimulation of the 'fight-or-flight' response, and that simultaneous activation of multiple intracellular signalling pathways contributes to this response. Data obtained under several conditions at the subcellular, microscopic level were consistent with results obtained at the cellular level. The results provide insight into regulation of cardiac calcium release and how alterations to this process may increase arrhythmia risk under different conditions. Time-dependent refractoriness of calcium (Ca(2+)) release in cardiac myocytes is an important factor in determining whether pro-arrhythmic release patterns develop. At the subcellular level of the Ca(2+) spark, recent studies have suggested that recovery of spark amplitude is controlled by local sarcoplasmic reticulum (SR) refilling whereas refractoriness of spark ...Continue Reading
References
Method for isolation of adult mouse cardiac myocytes for studies of contraction and microfluorimetry
Ca2+/calmodulin-dependent protein kinase II phosphorylation regulates the cardiac ryanodine receptor
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