The endothelium controls vascular tone by releasing various
vasoactive substances. Additionally, another pathway associated
with the hyperpolarization of both endothelial and vascular smooth
muscle cells contributes also to endothelium-dependent relaxations
(EDHF-mediated responses). These responses involve an increase in
the intracellular Ca concentration of the endothelial cells
followed by the opening of Ca-activated K channels of small and
intermediate conductances (SKCa and IKCa). These channels show a
distinct subcellular distribution, suggesting that their activation
could be elicited by distinct stimuli. Following KCa activation,
the endothelial hyperpolarization can be conducted to the
underlying smooth muscle cells by electrical coupling through
myo-endothelial gap junctions. In addition, the potassium efflux
can lead to the accumulation of potassium ions in the intercellular
space and the subsequent activation of smooth muscle Kir2.1 and/or
Na/K-ATPase. The hyperpolarization of the smooth muscle cells
produces vascular relaxation, predominantly by closing
voltage-gated calcium channels, and vasodilatation. EDHFmediated
responses are altered in various pathologies or, conversely, act as
a compensating mechanism when other endothelial pathways are
impaired. A better characterization of EDHF-mediated responses
should allow determining whether or not new drugable targets can be
identified within this endothelial pathway for the treatment of
cardiovascular diseases. Table of Contents: Endothelium-Dependent
Hyperpolarizations: The Classical "EDHF" Pathway / Conclusion /
References
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