Figure 1.

A: A schematic illustration of the fine structure of the diastolic depolarization (DD) of spontaneous action potential in rabbit SANC shown together with inward ion currents assessed in the study by Du and Nathan [1] and related Ca²⁺ signals (see text for detail). The nonlinear, exponentially rising, late DD part is shown as a gray area between membrane potential curve and an extrapolation of the initial, linear DD part. The action potential shapes are taken from the two first action potentials presented in Fig.1A of the study by Du and Nathan [1]. B: The ‘‘ischemic’’ solution mainly reduces the nonlinear, late DD part (c), rather than the early part (b) of the DD. Shown is a copy of the Figure 1G from [1]. C: Spontaneous beating of rabbit SANC critically depends upon Ca²⁺ related mechanisms and protein phosphorylation. Bars show a decrease in the beating rate (% control) induced by different drugs that affect Ca²⁺ cycling [ryanodine (Ry), BAPTA-AM], NCX (Li⁺ substitution for Na⁺), protein phosphorylation (PKI, H-89, MDL), or ion currents: I_f (Cs+) or T-type Ca2+ current (Ni⁺). From [6]. PKI and H-89 are protein kinase A inhibitors and MDL is an adenylyl cyclase inhibitor.