Gap junctions: functional effects of molecular structure and tissue distribution.
Abnormal conduction is fundamental to the pathogenesis of both atrial fibrillation and ventricular tachycardia/fibrillation. Normal atrial and ventricular myocytes express different combinations of multiple gap junction channel proteins and are interconnected by gap junctions in markedly different spatial distributions. These observations suggest that the disparate anisotropic conduction properties of atrial and ventricular muscle are determined, in part, by both structural and molecular features of gap junctions. Alterations in gap junctional coupling likely contribute to conduction abnormalities underlying reentrant atrial or ventricular arrhythmias.
Saffitz
J E
JE
Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.
D000818:Animals; D017630:Connexins / Q000032:analysis / Q000235:genetics; D004285:Dogs; D017629:Gap Junctions / Q000502:physiology* / Q000648:ultrastructure*; D015870:Gene Expression; D006325:Heart Atria / Q000378:metabolism / Q000648:ultrastructure; D006329:Heart Conduction System / Q000648:ultrastructure*; D006352:Heart Ventricles / Q000378:metabolism / Q000648:ultrastructure; D007150:Immunohistochemistry; D008958:Models, Molecular; D009206:Myocardium / Q000648:ultrastructure*; D010641:Phenotype; D012333:RNA, Messenger / Q000032:analysis
D017630:Connexins; D012333:RNA, Messenger