Key result
Endothelins act as local cytokines modifying cardiac contractility and hypertrophic myocardial wall remodeling.
Provides foundational insights into the autocrine and paracrine roles of endothelins in myocardial function and pathological remodeling.
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Endothelins may influence contractility and remodeling in hypertrophy; leaves open targeted therapies pending prospective validation.
There is growing evidence to support the existence of a dynamic interaction in vivo between cardiac myocytes and adjacent microvascular endothelial cells in the regulation of both cardiac myocyte and possibly endothelial cell phenotype and function. Endothelins may be only one of several endogenous cytokines or autocoids that are released by the cardiac microvascular and/or endocardial endothelium and transported vectorially to adjacent myocytes that could modify cardiac contractile state, perhaps in response to changes in microvascular blood flow. Similarly, cardiac myocytes themselves could release cytokines that could directly affect endothelial cell proliferation or angiogenesis and indirectly elicit or modify the release of endothelium-derived cytokines and autocoids. Thus, in addition to modifying function, endothelial cell-cardiac myocyte interactions may also be of importance in the dynamic events that lead to myocardial wall remodeling and angiogenesis during hypertrophic growth and in the response to cardiac injury.
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Krämer et al. (1992) reported a review. Endothelins was evaluated. Endothelins act as locally released cytokines that modify cardiac contractile state and may be important in myocardial wall remodeling during hypertrophic growth.
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