Status
Please wait ...

Details for messenger / hormone: EETs

EndoNet ID: ENH00961

To link to the content of EndoNet use the EndoNet ID that is given on the detail pages in the format ENX0000, where X is a place holder for the type of the component (e. g. R for receptor or C for anatomical structure).
As URL for the linking append this ID to the detail page for this type of component.
For an hormone that would be:

http://endonet.bioinf.med.uni-goettingen.de/hormone/ENH00000

It is also possible to use the search of EndoNet to link to the right detail page. The URL should look like

http://endonet.bioinf.med.uni-goettingen.de/search/ENC00000
If the search pattern is unambigious the user is directed to the corresponding detail page.

Synonyms

  • EETs
  • EDHFs
  • endothelium-derived hyperpolarizing factors
  • epoxyeicosatrienoic acids

General information

  • There are 3 principal mechanisms linked to the EDHF phenomenon: (1) an increase in endothelial [Ca2+] following cell stimulation triggers the synthesis of a CYP metabolite, which is essential for the subsequent EDHF-mediated responses; (2) K+, released from endothelial cells via Ca2+-dependent K+-channels, induces smooth muscle hyperpolarization by activating inwardly rectifying K+ channels and/or the Na+/K+-ATPase on vascular smooth muscle cells; and (3) endothelial cell hyperpolarization is transmitted to the vascular smooth muscle via gap junctions. [1]
  • EETs are arachidonic acid epoxides, and in mammals the epoxidation of polyunsaturated fatty acids to cis-epoxides is unique to the CYP enzyme system. [1]
  • EETs and their metabolites are potent vasodilators and are able to hyperpolarize both endothelial and vascular smooth muscle cells by activating Ca2+-dependent K+ channels. [1]
  • EETs are degraded by the soluble epoxide hydrolase as well as by β-oxidation, the exception being 5,6-EET, which is more rapidly metabolized by COX. [1]
  • Both 11,12- and 14,15-EET activate one or more metalloproteases and enhance endothelial cell migration as well as the release of HB-EGF from the cell surface. [1]
  • EETs released from astrocytes increase thymidine incorporation into endothelial cells and elicite the formation of capillary like structures. [1]
  • The CYP 2C8 and 2C9 promoters contain a glucocorticoid-responsive element that is recognized and transactivated by glucocorticoid receptor. Identification of this functional element provides a rational mechanistic basis for the induction of CYP 2C protein and an increase in EDHF-mediated responses in porcine coronary arteries by cortisol. [1]
  • EETs are also able to transactivate the EGF receptor in endothelial cells, and the activation of this particular signaling pathway has been linked to cell proliferation and angiogenesis. [1]
  • Multiple CYP enzymes are capable of generating EETs including members of the CYP 1A, CYP 2B, CYP 2C, CYP 2D, CYP 2J, and CYP 4A subfamilies. [1]
  • Mediate the NO- and prostacyclin (PGI2)-independent vasodilator responses in different arteries. [1]

Classification

Hormone function

  • homeostasis
    • cardiovascular control
      • ion flow control

      Chemical classification

      • hormone
        • not genome-encoded
          • eicosanoids/fatty acid derivatives

      Composition

      Links to other resources

      • Anatomical structure: continuous_vascular_endothelial_cell_of_blood_vessels_and_lymphatics

      Targets

      Cell
      No records found.
      Reference