Summary
Based on current evidence, the term of endothelium-derived hyperpolarising factor should represent a mechanism rather than a specific factor. The mechanism(s) of endothelium-dependent hyperpolarization (i.e., EDHF-mediated relaxation) seems to be heterogeneous depending on several factors (e.g. size and vascular bed), surrounding environment (oxidative stress, hypercholesterolemia) and demand (compensatory). Different endothelial mediators or pathways involved in EDHF-mediated relaxation may also work simultaneously and/or substitute each others. It implies a reasonable physiological sense, although to some extend and when EDHF acts as backup mechanism for endothelium-dependent relaxation in the present of compromised NO contribution. Thus, alternatives for EDHF-typed responses (H2O2, K+ etc.) will provide a guarantee for compensation of endothelial function. However, once the involvement of a certain endothelium-derived vasodilator for a given vascular bed is confirmed, it should preferably be described by their proper name (i.e., endothelium-derived H2O2, or CNP), and no longer be termed as “EDHF”. Although the role of EDHF in the genesis of Cardiovascular Disease remains to be further elucidated, the EDHF contribution and its importance at the level of small arteries delivers a theoretical opportunity to control systemic blood pressure. There is an increasing experimental evidence to suggest that treatment of the EDHF system could provide a means to control blood pressure and blood flow to target organs in compatible way achieved by manipulations of NO system.
Finally, since “EDHF story” is particularly heterogeneous and mainly based on animal studies, the most important and demanding current task is to strengthen our knowledge about EDHF action in human arteries in health and disease.
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