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Physiological Reviews, Vol. 83, No. 1, January 2003, pp. 59-115; 10.1152/physrev.00017.2002.
Copyright ©2003 by the American Physiological Society
University of Antwerp, Antwerp, Belgium
Brutsaert, Dirk L.
Cardiac Endothelial-Myocardial Signaling: Its Role in
Cardiac Growth, Contractile Performance, and Rhythmicity. Physiol. Rev. 83: 59-115, 2003.
Experimental work during the past 15 years
has demonstrated that endothelial cells in the heart play an obligatory
role in regulating and maintaining cardiac function, in particular, at the endocardium and in the myocardial capillaries where endothelial cells directly interact with adjacent cardiomyocytes. The emerging field of targeted gene manipulation has led to the contention that
cardiac endothelial-cardiomyocytal interaction is a prerequisite for normal cardiac development and growth. Some of the
molecular mechanisms and cellular signals governing this interaction,
such as neuregulin, vascular endothelial growth factor, and
angiopoietin, continue to maintain phenotype and survival of
cardiomyocytes in the adult heart. Cardiac endothelial cells, like
vascular endothelial cells, also express and release a variety of auto-
and paracrine agents, such as nitric oxide, endothelin, prostaglandin
I2, and angiotensin II, which directly influence cardiac
metabolism, growth, contractile performance, and rhythmicity of the
adult heart. The synthesis, secretion, and, most importantly, the
activities of these endothelium-derived substances in the heart are
closely linked, interrelated, and interactive. It may therefore be
simplistic to try and define their properties independently from one
another. Moreover, in relation specifically to the endocardial
endothelium, an active transendothelial physicochemical gradient for
various ions, or blood-heart barrier, has been demonstrated.
Linkage of this blood-heart barrier to the various other
endothelium-mediated signaling pathways or to the putative vascular
endothelium-derived hyperpolarizing factors remains to be
determined. At the early stages of cardiac failure, all major
cardiovascular risk factors may cause cardiac endothelial activation as
an adaptive response often followed by cardiac endothelial dysfunction.
Because of the interdependency of all endothelial signaling pathways,
activation or disturbance of any will necessarily affect the others
leading to a disturbance of their normal balance, leading to further
progression of cardiac failure.
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