Developmental changes in ionic channel activity in the embryonic murine heart

MP Davies, RH An, P Doevendans, S Kubalak… - Circulation …, 1996 - Am Heart Assoc
MP Davies, RH An, P Doevendans, S Kubalak, KR Chien, RS Kass
Circulation research, 1996Am Heart Assoc
We have isolated murine embryonic atrial and ventricular cells derived from timed-pregnant
females at different periods and used patch-clamp procedures to investigate age-and
chamber-specific expression of ionic channels in the developing fetal mouse. Our data
indicate that L-type Ca2+ channels play a dominant role in excitation during early murine
cardiac embryogenesis and that Na+ channel expression increases dramatically just before
birth. K+ channel expression is particularly sensitive to changes during development …
Abstract
We have isolated murine embryonic atrial and ventricular cells derived from timed-pregnant females at different periods and used patch-clamp procedures to investigate age- and chamber-specific expression of ionic channels in the developing fetal mouse. Our data indicate that L-type Ca2+ channels play a dominant role in excitation during early murine cardiac embryogenesis and that Na+ channel expression increases dramatically just before birth. K+ channel expression is particularly sensitive to changes during development. Neither atrial nor ventricular cells express a slowly activating component of delayed rectification (IKs) until just before birth, and inwardly rectifying channel activity, associated with determination of cellular resting potential, is not markedly apparent until late stages of embryogenesis. Instead, we find robust expression of the ATP-regulated K+ channel at early and late stages of embryonic development, which may indicate a novel functional role for this channel during morphogenesis of the heart. These results have important implications for the physiology and development of the murine cardiac conduction system and will also serve as a baseline for future studies designed to investigate developmental changes of ion channel expression in the myocardium of both wild-type and genetically modified mice.
Am Heart Assoc