Epoxyeicosatrienoic acids, potassium channel blockers and endothelium‐dependent hyperpolarization in the guinea‐pig carotid artery

@article{Chataigneau1998EpoxyeicosatrienoicAP,
  title={Epoxyeicosatrienoic acids, potassium channel blockers and endothelium‐dependent hyperpolarization in the guinea‐pig carotid artery},
  author={T. Chataigneau and M. F{\'e}l{\'e}tou and J. Duhault and P. Vanhoutte},
  journal={British Journal of Pharmacology},
  year={1998},
  volume={123}
}
Using intracellular microelectrodes, we investigated the effects of 17‐octadecynoic acid (17‐ODYA) on the endothelium‐dependent hyperpolarization induced by acetylcholine in the guinea‐pig isolated internal carotid artery with endothelium. In the presence of Nω‐nitro‐L‐arginine (L‐NOARG, 100 μM) and indomethacin (5 μM) to inhibit nitric oxide synthase and cyclo‐oxygenase, acetylcholine (1 μM) evoked an endothelium‐dependent hyperpolarization which averaged −16.4 mV starting from a resting… Expand
Role of SKCa and IKCa in endothelium‐dependent hyperpolarizations of the guinea‐pig isolated carotid artery
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TLDR
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TLDR
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TLDR
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TLDR
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Endothelium‐dependent relaxations are attributed to the release of various factors, such as nitric oxide, carbon monoxide, reactive oxygen species, adenosine, peptides and arachidonic acidExpand
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References

SHOWING 1-10 OF 41 REFERENCES
Inhibitors of the cytochrome P450‐mono‐oxygenase and endothelium‐dependent hyperpolarizations in the guinea‐pig isolated carotid artery
TLDR
The results suggest that in guinea‐pig carotid artery, the metabolism of arachidonic acid, either through cyclo‐oxygenase, lipoxygenases or cytochrome p450 mono‐oxyGENase, is not involved in acetylcholine‐induced endothelium‐dependent hyperpolarizations. Expand
Endothelium‐derived factors and hyperpolarization of the carotid artery of the guinea‐pig
TLDR
Transmembrane potentials were recorded from isolated carotid arteries of the guinea‐pig supervised with modified Krebs‐Ringer bicarbonate solution and acetylcholine induced hyperpolarization was not affected by the addition of indomethacin. Expand
Role of potassium channels in endothelium‐dependent relaxation resistant to nitroarginine in the rat hepatic artery
TLDR
It is proposed that endothelial cell activation induces secretion of an endothelium‐derived hyperpolarizing factor(s) (EDHF), distinct from NO and cyclo‐oxygenase products, which activates more than one type of K‐channel on the smooth muscle cells. Expand
Characterization of the potassium channels involved in EDHF‐mediated relaxation in cerebral arteries
TLDR
KV, but not KATP and BKCa, is involved in the EDHF‐mediated relaxation in the guinea‐pig basilar artery, and the synergistic action of apamin and ciclazindol could indicate that both KV and SKCa are activated by EDHF. Expand
Apamin‐sensitive K+ channels mediate an endothelium‐dependent hyperpolarization in rabbit mesenteric arteries.
TLDR
The results suggest that ACh stimulates M3 receptors on endothelial cells, triggering the release of nitric oxide and prostanoids, which hyperpolarize underlying smooth muscle by activation of KATP channels, and therelease of an EDHF, whichhyperpolarizes smooth muscle through the activation of apamin‐sensitive K+ (KAS) channels. Expand
Evidence Against the Involvement of Cytochrome P450 Metabolites in Endothelium‐Dependent Hyperpolarization of the Rat Main Mesenteric Artery
TLDR
The results do not support the view that the ACh‐induced endothelium‐dependent hyperpolarization in the rat mesenteric artery is mediated by cytochrome P450 mono‐oxygenase metabolites. Expand
Effects of cytochrome P450 inhibitors on EDHF‐mediated relaxation in the rat hepatic artery
TLDR
The lack of effect of 17‐ODYA on relaxations mediated by EDHF, together with the failure of extracellularly‐applied EETs to produce relaxation, collectively suggest that EDHF is not an EET in the rat hepatic artery. Expand
A transferable, beta‐naphthoflavone‐inducible, hyperpolarizing factor is synthesized by native and cultured porcine coronary endothelial cells.
TLDR
The findings suggest that the vascular endothelium releases a transferable hyperpolarizing factor, chemically distinct from NO and prostacyclin, in response to agonists and mechanical stimulation. Expand
Identification of epoxyeicosatrienoic acids as endothelium-derived hyperpolarizing factors.
TLDR
Data support the hypothesis that the EETs are EDHFs, which causes endothelium-dependent relaxations of coronary arteries through its metabolism to epoxyeicosatrienoic acids by cytochrome P450 by boosting the open-state probability of a Ca2+-activated K+ channel in coronary smooth muscle cells. Expand
Evidence against a role of cytochrome P450‐derived arachidonic acid metabolites in endothelium‐dependent hyperpolarization by acetylcholine in rat isolated mesenteric artery
TLDR
The results suggest that the contribution of a cytochrome P450‐derived metabolite of arachidonic acid to ACh‐induced hyperpolarization via EDHF release is minimal or absent in rat mesenteric artery. Expand
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