Developmental Changes in the Excitation–Contraction Mechanisms of the Ventricular Myocardium and Their Sympathetic Regulation in Small Experimental Animals

Figure 1. Action potentials of the guinea pig and mouse ventricle. Recordings were obtained in the guinea pig (A) and mouse (B) at fetal (a) neonatal (b) and adult (c) stages.

Figure 2. A schematic diagram of developmental and pathological changes in the excitation–contraction coupling of mouse ventricular cardiomyocytes. Fetus: The action potential triggers sarcolemmal Ca2+ influx through voltage-dependent Ca2+ channels, and a part of the Ca2+ diffuses towards the cell center and triggers Ca2+-induced Ca2+ release from Ca2+ release channels (ryanodine receptors) on the slightly present SR. Neonate: Partially developed T-tubular invaginations cause Ca2+-induced Ca2+ release from the coupled release channels on the SR. The released Ca2+ then triggers Ca2+ release from the neighboring Ca2+ release sites, uncoupled from the T-tubules. Adult: A well-developed T-tubular network enables simultaneous Ca2+ release from the SR in the entire cell on an action potential. Diseased: The T-tubule-SR coupling is partly disrupted and the SR Ca2+ release pattern resembles that in the immature myocardium.

Figure 3. α-Adrenoceptor-mediated inotropy in the right ventricle. (A) Adult guinea pig showing positive inotropy. (B) Neonatal (a), 2-week-old (b), and 4-week-old mice (c). The inotropy changes from positive to negative during postnatal development. (C) Neonatal mice in the presence of nifedipine (a), 4-week-old mice in the presence of SEA0400 (b). The positive and negative inotropy was inhibited by nifedipine and SEA0400, respectively. Arrows indicate α-adrenergic stimulation by phenylephrine in the presence of propranolol.