Fig. 5. Reciprocal signaling between cardiac endothelial cells and cardiomyocytes influences myocardial growth, contractile performance, and rhythmicity.

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Fig. 5. Reciprocal signaling between cardiac endothelial cells and cardiomyocytes influences myocardial growth, contractile performance, and rhythmicity. MyoCapE interacts with cardiomyocytes through autocrine-paracrine coupling and growth peptide signaling. The EE may, in addition, act through an active blood-heart barrier mechanism. EE cell-to-cell coupling through gap junction allows for rapid electrochemical intercellular spreading and amplification of functional properties. Tight junctions and zonula adherens participate in the control of trans-EE-permeability through overlapping intercellular clefts. The Purkinje fiber network and the subendocardial neural plexus (SNP) run immediately subjacent to the EE and may further endorse endothelial control of cardiac rhythmicity. Et-1, endothelin-1; NO, nitric oxide; PGI2, prostacyclin; AI and AII, angiotensins I and II; VEGF, vascular endothelial growth factor. DOI: (10.1152/physrev.00017.2002)