Abstract
Endothelium lining the coronary vasculature and the heart chambers is a dynamic sensor that serves a variety of functions including bidirectional communications with cardiac myocytes. Among endothelium-released factors, nitric oxide exerts multifactorial effects on various cell types in the heart and may play a role in growth of the vasculature and myocardial hypertrophy. This review summarizes new data regarding the endothelium-to-myocyte signaling focusing on its role in regulation of cardiac hypertrophy through a nitric-oxide-mediated paracrine signal.
MeSH terms
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Animals
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Blood Coagulation Factors / metabolism
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Cardiomegaly / metabolism*
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Coronary Circulation*
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Endothelins / metabolism
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Endothelium, Vascular / metabolism*
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Fibroblast Growth Factors / metabolism
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Humans
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Ion Channel Gating
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Myocardium / metabolism*
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Myocytes, Cardiac / metabolism
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Nitric Oxide / metabolism*
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Nitric Oxide Synthase Type I / metabolism
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Nitric Oxide Synthase Type III / metabolism
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Paracrine Communication
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Platelet-Derived Growth Factor / metabolism
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Prostaglandins / metabolism
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Signal Transduction
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Vascular Endothelial Growth Factors / metabolism
Substances
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Blood Coagulation Factors
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Endothelins
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Platelet-Derived Growth Factor
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Prostaglandins
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Vascular Endothelial Growth Factors
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Nitric Oxide
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Fibroblast Growth Factors
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Nitric Oxide Synthase Type I
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Nitric Oxide Synthase Type III