Age-related changes in gap junctional protein of the rat heart.

Gap junctions are composed of narrow membrane channels that permit the passage of ions and small molecules between the cytoplasmic compartments of abutting cells. Intracellular communication via these gap junctional channels has been proposed to contribute to a diverse range of physiological processes such as tissue homeostasis, growth regulation and development (1). Morphogenetic signals are thought to be among the small molecules that diffuse intercellularly via the gap junction. In the neonate and adult heart, developmental changes in myocardial gap junction distribution have been reported (2). Disruptions of the distribution and tissue content of connexin 43 (Cx43) gap junctions leading to impaired intracellular conduction have been reported to predispose the heart to reentry arrhythmias in infarct border zones (3) and in reversibly ischemic myocardium. Abnormal impulse propagation resulting from changes of the gap junction may contribute to the electromechanical dysfunction associated with hibernation (4). The aim of the present study was to characterize gap junction organization in aged ventricular myocardium and to establish whether abnormalities exist in the myocardium of aged hearts (5).