Ontogeny of excitation-contraction coupling in the mammalian heart.
The neonate mammalian heart is phenotypically different from the adult heart in many respects. Understanding these phenotypic differences are a fundamental component of understanding the mechanisms of congenital heart disease and its treatment. Differences in excitation-contraction (E-C) coupling of the neonatal heart from that of the adult include less reliance on intercellular sources of Ca(2+) such as that from sarcoplasmic reticulum (SR). Electron micrographs indicate that these immature cardiomyocytes lack transverse tubules and the SR is sparse. This paper focuses on the changes in the phenotype of E-C coupling during ontogeny in the mammalian heart and the molecular mechanisms underlying these changes.
Tibbits
Glen F
GF
Cardiac Membrane Research Laboratory, Simon Fraser University, Burnaby, BC, V5A 1S6, Canada. tibbits@sfu.ca
Xu
Liqun
L
Sedarat
Franklin
F
D000818:Animals; D000831:Animals, Newborn; D020746:Calcium Channels, L-Type / Q000502:physiology; D020013:Calcium Signaling / Q000502:physiology; D006321:Heart / Q000254:growth & development* / Q000502:physiology*; D006329:Heart Conduction System / Q000502:physiology; D008322:Mammals / Q000254:growth & development / Q000502:physiology; D009200:Myocardial Contraction / Q000502:physiology*; D019837:Ryanodine Receptor Calcium Release Channel / Q000502:physiology; D019831:Sodium-Calcium Exchanger / Q000502:physiology
D020746:Calcium Channels, L-Type; D019837:Ryanodine Receptor Calcium Release Channel; D019831:Sodium-Calcium Exchanger