Differences in the control of basal L-type Ca2+ current by the cyclic AMP signaling cascade in frog, rat, and human cardiac myocytes

beta-adrenergic receptors (beta-ARs) mediate the positive inotropic effects of catecholamines by cAMP-dependent phosphorylation of the L-type Ca2+ channels (LTCCs), which provide Ca2+ for the initiation and regulation of cell contraction. The overall effect of cAMP-modulating agents on cardiac calcium current (I (Ca,L)) and contraction depends on the basal activity of LTCCs which, in turn, depends on the basal activities of key enzymes involved in the cAMP signaling cascade. Our current work is a comparative study demonstrating the differences in the basal activities of beta-ARs, adenylyl cyclase, phosphodiesterases, phosphatases, and LTCCs in the frog and rat ventricular and human atrial myocytes. The main conclusion is that the basal I (Ca,L), and consequently the contractile function of the heart, is secured from unnecessary elevation of its activity and energy consumption at the several checking-points of cAMP-dependent signaling cascade and the loading of these checking-points may vary in different species and tissues.