Sympathetic Potentiation of Cyclic ADP-Ribose Formation in Rat Cardiac Myocytes
Sympathetic nerve excitation stimulates β-adrenergic receptors on cardiac myocytes by release of noradrenaline, leading to an increase in the contractility. This cardiostimulant effect is mediated by an increase in Ca2+ permeability resulted from cyclic AMP-dependent phosphorylation of voltage-gated ion channels (Figure 1). Opening of phosphorylated L-type Ca2+ channels and tetrodotoxin-sensitive Na+ channels results in a transient intracellular Ca2+ concentration increase ([Ca2+]i transient) which is greater than without sympathetic stimulation. The increased [Ca2+]i is further amplified by Ca2+-induced Ca2+-release (CICR) from the sarcoplasmic reticulum ryanodine receptor Ca2+ release channels, leading to strengthened contraction. In CICR in the heart, both cyclic ADP-ribose (cADP-ribose) and Ca2+ cooperatively activate type-II ryanodine receptors to release Ca2+. However, no information on the concentration of cADP-ribose after β-adrenoceptor stimulation has yet been reported (Figure 2).
KeywordsAdrenergic Receptor Ventricular Myocytes Ryanodine Receptor ADRENOCEPTOR Stimulation Adrenergic Receptor Subtype
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