The other endothelium-derived relaxing factor

A review of recent findings concerning the nature and cellular actions of endothelium-derived hyperpolarizing factor (EDHF)

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Abstract

We can anticipate that within the next two to three years considerably more information will become available concerning the nature of EDHF. Over the past five years, much progress has been made which leads the authors of this review to conclude that there are likely several distinct EDHF molecules. Thus, the data that we have reviewed concerning the nature of EDHF cannot be readily reconciled with the hypothesis that there is only one molecular species. Should there be more than one EDHF and, in particular, if the expression of different EDHFs shows vascular bed specificity (i.e. differences between cerebral versus mesenteric) then the potential exists for selective pharmacological manipulation. As we have stressed in our review, it is very important that the contribution of myo-endothelial cell gap junctions to endothelium-dependent hyperpolarization be thoroughly investigated. A very recent report by Edwards et al |83| suggests that the role of myo-endothelial cell junctions varies considerably from one vessel bed to another. Edwards et al 831 compared responses putatively mediated by EDHF in guinea-pig internal carotid and rat hepatic and mesenteric arteries and studied the effects of the gap-junction inhibitors carbenoxolone and Gap 27. Their data suggest that gap junctions play some role in the response to EDHF in the rat vessels, however, the primary mechanism for EDHF would appear to be mediated by K+. In contrast, in the guinea-pig internal carotid artery, gap junctions would appear to be the primary, if not sole, mechanism. Clearly more studies need to be performed, however, it is apparent that there is considerable heterogeneity with respect to the mechanisms that mediate endothelium-dependent hyperpolarization in different vascular beds. Some of these differences may be species-dependent but others may relate to vessel specialization.

Original languageEnglish
Pages (from-to)119-129
Number of pages11
JournalBiomedical Research (India)
Volume11
Issue number2
Publication statusPublished - 2000
Externally publishedYes

Fingerprint

Endothelium-Dependent Relaxing Factors
Endothelial cells
Endothelium
Rats
Carbenoxolone
Gap Junctions
Molecules
Intercellular Junctions
Blood Vessels
Guinea Pigs
Endothelial Cells
Mesenteric Arteries
Hepatic Artery
Internal Carotid Artery
Pharmacology
endothelium-dependent hyperpolarization factor

Keywords

  • Arachidonic acid
  • Cannabinoids
  • Cytochrome P450
  • Endothelium
  • Endothelium-derived hyperpolarizing factor
  • Gap junctions
  • Nitric oxide
  • Potassium channels

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

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title = "The other endothelium-derived relaxing factor: A review of recent findings concerning the nature and cellular actions of endothelium-derived hyperpolarizing factor (EDHF)",
abstract = "We can anticipate that within the next two to three years considerably more information will become available concerning the nature of EDHF. Over the past five years, much progress has been made which leads the authors of this review to conclude that there are likely several distinct EDHF molecules. Thus, the data that we have reviewed concerning the nature of EDHF cannot be readily reconciled with the hypothesis that there is only one molecular species. Should there be more than one EDHF and, in particular, if the expression of different EDHFs shows vascular bed specificity (i.e. differences between cerebral versus mesenteric) then the potential exists for selective pharmacological manipulation. As we have stressed in our review, it is very important that the contribution of myo-endothelial cell gap junctions to endothelium-dependent hyperpolarization be thoroughly investigated. A very recent report by Edwards et al |83| suggests that the role of myo-endothelial cell junctions varies considerably from one vessel bed to another. Edwards et al 831 compared responses putatively mediated by EDHF in guinea-pig internal carotid and rat hepatic and mesenteric arteries and studied the effects of the gap-junction inhibitors carbenoxolone and Gap 27. Their data suggest that gap junctions play some role in the response to EDHF in the rat vessels, however, the primary mechanism for EDHF would appear to be mediated by K+. In contrast, in the guinea-pig internal carotid artery, gap junctions would appear to be the primary, if not sole, mechanism. Clearly more studies need to be performed, however, it is apparent that there is considerable heterogeneity with respect to the mechanisms that mediate endothelium-dependent hyperpolarization in different vascular beds. Some of these differences may be species-dependent but others may relate to vessel specialization.",
keywords = "Arachidonic acid, Cannabinoids, Cytochrome P450, Endothelium, Endothelium-derived hyperpolarizing factor, Gap junctions, Nitric oxide, Potassium channels",
author = "Hong Ding and John McGuire and Christopher Triggle",
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AU - Triggle, Christopher

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