Vascular endothelial cell-cardiac myocyte crosstalk in achieving a balance between energy supply and energy use.
In isolated perfused hearts, endothelial cells in the coronary arterial vascular system release substances that can alter the contractility of the cardiac myocytes. There are at least two different substances, one that increases and another that decreases the contractility of cardiac myocytes. The rate of release of these endothelial-derived cardioactive substances depends on the oxygen tension in the immediate vicinity of the cardiac myocytes. As the local oxygen tension increases the contractility changes in the same direction. The oxygen sensor in this regulatory system is the cardiac myocyte, which then releases substances that regulate the secretion of endothelin and a relaxant by endothelial cells. The result is a loop involving cross talk between coronary endothelial cells and cardiac myocytes to modulate cardiac contractility in accordance with the oxygen supply to the cardiac myocytes. Preliminary data suggest that the change in contractility is related to a change in structure and position of the cross bridge due to phosphorylation of a protein in the thick filament.
Winegrad
S
S
Department of Physiology, School of Medicine, University of Pennsylvania, Philadelphia, USA.
Henrion
D
D
Rappaport
L
L
Samuel
J L
JL
D000818:Animals; D002450:Cell Communication / Q000502:physiology; D003331:Coronary Vessels / Q000502:physiology*; D004730:Endothelium, Vascular / Q000502:physiology*; D004734:Energy Metabolism; D006321:Heart / Q000502:physiology*; D006801:Humans; D009200:Myocardial Contraction