Inositol‐1,4,5‐trisphosphate induced Ca²⁺ release and excitation–contraction coupling in atrial myocytes from normal and failing hearts

Abstract

Key pointsr Impaired calcium (Ca 2+ ) signalling is the main contributor to depressed ventricular contractile function and occurrence of arrhythmia in heart failure (HF). waves resulted from the combined action of enhanced IICR and increased activity of sarcolemmal Na + -Ca 2+ exchange depolarizing the cell membrane. In conclusion, the data support the hypothesis that in atrial myocytes from hearts with left ventricular failure, enhanced CaTs during ECC exert positive inotropic effects on atrial contractility which facilitates ventricular filling and contributes to maintaining cardiac output. However, HF atrial cells were also more susceptible to developing arrhythmogenic Ca 2+ waves which might form the substrate for atrial rhythm disorders frequently encountered in HF.

Heterogeneity of transverse-axial tubule system in mouse atria: Remodeling in atrial-specific Na + –Ca 2+ exchanger knockout mice

“…The absence of TATs is thought to be responsible for the non-uniform Ca release pattern observed in atrial cells from rats [5–8], cats [9], rabbits [10,11] and guinea pigs [12]. Without the TAT network, couplons can only be formed at the periphery or subsarcolemmal (SS) space where the LCCs on the surface membrane are found in close proximity to RyRs on the SR membrane.…”

Disorders of Ca2+ handling and cell-to-cell coupling are implicated in the development of acute heart failure in intact animal hearts: An ultrastructural study

“…In such conditions, the contractile units (sarcomeres) are in synchrony, as shown in Figures 1A and 1B. Calcium is crucial in normal cardiac contraction, while disturbances of excitation-contraction coupling result in both contractile dysfunction and arrhythmogenesis, particularly in cardiac disease but also in acute heart failure (35). The latter is supported by our study demonstrating disturbances in synchronized contraction ( Figures 1D, 2A, 2C and 2E) and cardiac cell-to-cell communication (Figures 3 and 4) in the setting of K + deficiency, increased levels of catecholamines or abnormally fast beating rates.…”

IP3 and Ca2+ signals in the heart: boost them or bust them?

“…How potential Ca 2+ signalling complications arising from this constellation could be avoided by spatially targeting the IP 3 R expression and by finely tuning their activity can be conceptualized based on findings published in this issue of The Journal of Physiology (Hohendanner et al . ).…”