Intracellular calcium homeostasis in cardiac myocytes.

Abstract

Calcium homeostasis in cardiac myocytes results from the integrated function of transsarcolemmal Ca2+ influx and efflux pathways modulated by membrane potential and from intracellular Ca2+ uptake and release caused predominantly by SR function. These processes can be importantly altered in different disease states as well as by pharmacological agents, and the resulting changes in systolic and diastolic [Ca2+]i can cause clinically significant alterations in contraction and relaxation of the heart. It may be anticipated that a rapid increase in our understanding of the pathophysiology of Ca2+ homeostasis in cardiac myocytes will be forthcoming as the powerful new tools of molecular and structural biology are used to investigate the regulation of Ca2+ transport systems.

Ambulatory blood pressure and left ventricular structure and function in relation to the G-protein β3-subunit polymorphism C825T in White Europeans

“…In cardiomyocytes, the extrusion and sequestration of free calcium during diastole is dependent on cyclic AMP, is modulated by b-receptors, and is influenced by several ion transport mechanisms including the Na + /H + exchanger. [30][31][32][33][34][35][36] Cardiac b-receptors couple to a G-protein-stimulated adenylcyclase, which in turn stimulates cyclic AMP-dependent regulatory mechanisms. 30,31,33,37 Recent studies in rodent cardiomyocytes revealed that b 2 -receptors couple to G-proteins, which lead to inhibition of cyclic AMP formation downstream.…”

“…[30][31][32][33][34][35][36] Cardiac b-receptors couple to a G-protein-stimulated adenylcyclase, which in turn stimulates cyclic AMP-dependent regulatory mechanisms. 30,31,33,37 Recent studies in rodent cardiomyocytes revealed that b 2 -receptors couple to G-proteins, which lead to inhibition of cyclic AMP formation downstream. 38,39 In the ischaemic myocardium, the Na + /H + exchanger, which itself is under the influence of the C825T polymorphism, 3,4 exerts an important modulatory action on cardiac excitation-contraction coupling.…”

Ca2+ Controls Functional Expression of the Cardiac K+ Transient Outward Current via the Calcineurin Pathway

“…pF, picofarads. exchanger working in the "reverse mode" (17). Even if small, the open probability of the L-type Ca 2ϩ channel at rest is not null as assessed by single channel recording (18).…”

Connexin 43 Hemichannels and Pharmacotherapy of Myocardial Ischemia Injury

“…Based on single Hc conductance measurements, it was suggested that opening of only 50 Hc is sufficient to drown the cell with Na + (John et al, 1999b). As a result, Na + overload induces the activation of reverse Na + -Ca ++ exchange and hence promotes intracellular Ca ++ accumulation (Barry & Bridge, 1993;Silverman & Stern, 1994), irreversible cell injury and arrhythmogenic transient inward currents (Tani & Neely, 1989). Altogether, these data endorse the theory of the involvement of the unapposed Hc in ischemic-induced injury and support our hypothesis that inhibition of Hc during ischemia is an important determinant for cardioprotection against ischemia/reperfusion injury.…”