Endothelium-derived hyperpolarizing factor, but not nitric oxide or prostacyclin release, is resistant to menadione-induced oxidative stress in the bovine coronary artery

@article{Kaw1999EndotheliumderivedHF,
  title={Endothelium-derived hyperpolarizing factor, but not nitric oxide or prostacyclin release, is resistant to menadione-induced oxidative stress in the bovine coronary artery},
  author={Semiko Kaw and Markus Hecker},
  journal={Naunyn-Schmiedeberg's Archives of Pharmacology},
  year={1999},
  volume={359},
  pages={133-139}
}
  • S. Kaw, M. Hecker
  • Published 25 January 1999
  • Biology, Chemistry
  • Naunyn-Schmiedeberg's Archives of Pharmacology
The interaction of superoxide anions (O2–) generated by menadione with the synthesis and/or action of nitric oxide (NO), prostacyclin (PGI2) and endothelium-derived hyperpolarizing factor (EDHF) was investigated in segments of the left anterior descending coronary artery (LAD) isolated from bovine hearts. EDHF and NO release were monitored by superfusion bioassay in segments pre-constricted with the thromboxane mimetic, U46619, PGI2 release in addition by enzyme immunoassay for 6-keto… 
Different Influences of Extracellular and Intracellular Superoxide on Relaxation Through the NO/sGC/cGMP Pathway in Isolated Rat Iliac Arteries
TLDR
It is suggested that extracellular superoxide reacts with NO only outside the cell, whereas intracellularsuperoxide not only scavenges NO inside the cell but also shifts the sGC redox equilibrium.
Opposite effects of endogenous nitric oxide and prostaglandin F2α in the rat mesenteric bed
TLDR
The present results suggest an opposite action between NO and PGF2 alpha on the NA-induced contractions in the rat mesenteric bed.
Effects of eicosanoids and nitric oxide on the noradrenaline-induced contractions in the rat mesenteric bed.
TLDR
Results show that metabolites of AA, through both the COX and the lipoxygenase pathways, are involved in the NA-induced contractions in the rat mesenteric bed.
Effects of Endothelium-Derived Hyperpolarizing Factor and Nitric Oxide on Endothelial Function in Femoral Resistance Arteries of Spontaneously Hypertensive Rats
TLDR
Evaluated femoral resistance arteries of hypertensive rats showed that endothelium-derived hyperpolarizing factor-induced dilatation was attenuated before the loss of NO-mediated vasodilatation in the femoral Resistance arteries of SHR and EDHF-mediated dilatations were attenuated in SHR but not in WKY.
Role of Calcium-Activated Potassium Channels in Impaired Acetylcholine Vasodilatory Responses in Diabetic Rats
TLDR
Insight is provided into the development and progression of altered diabetic vascular responses and it is demonstrated that an alternate pathway involving calcium-activated potassium channels may compensate for diminished nitric oxide bioactivity.
Nifedipine Increases Endothelial Nitric Oxide Bioavailability by Antioxidative Mechanisms
TLDR
It is concluded that the calcium antagonist nifedipine enhances the bioavailability of endothelial NO without significantly altering the NOS (type III) mRNA and protein expression, possibly via an antioxidative protection.
Vascular Consequences of Endothelial Nitric Oxide Synthase Uncoupling for the Activity and Expression of the Soluble Guanylyl Cyclase and the cGMP-Dependent Protein Kinase
TLDR
The present review summarizes current concepts concerning eNOS uncoupling and also focuses on the consequences for downstream signaling with respect to activity and expression of the sGC and cGK-I in various diseases.
Is hydrogen peroxide an EDHF in human radial arteries?
TLDR
The hypothesis that endogenously produced H2O2 mediated the nitric oxide/prostanoid-independent relaxation to carbachol in radial arteries obtained from patients undergoing coronary artery bypass surgery is examined to show blood vessels showing EDHF-mediated relaxations resistant to oxidative stress may provide favorable outcomes in revascularization surgery.
Non-esterified fatty acids impair endothelium-dependent vasodilation in rat mesenteric resistance vessels.
TLDR
It is concluded that NEFAs directly impair endothelial function in rat resistance arteries via an increase in oxidative stress at the vascular endothelium.
Endothelium-derived Hyperpolarizing Factor: A Cousin to Nitric Oxide and Prostacyclin
There is now strong evidence that an endothelial mechanism, other than nitric oxide or prostacyclin, exists for dilating arteries and arterioles. This third pathway has been named endothelium-derived
...
...

References

SHOWING 1-10 OF 29 REFERENCES
Nitric oxide attenuates the release of endothelium-derived hyperpolarizing factor.
TLDR
Findings indicate that under physiological conditions, the production of EDHF is damped by NO, and it follows that when NO synthesis is impaired, alleviation of this intrinsic inhibition may, at least in part, maintain endothelial vasodilator function.
Nitric oxide is the mediator of both endothelium-dependent relaxation and hyperpolarization of the rabbit carotid artery.
TLDR
The studies indicate that the release of NO by acetylcholine is only partially inhibited by these inhibitors of NO synthase when used even at high concentrations, and NO rather than another factor accounts fully for endothelium-dependent responses of the rabbit carotid artery.
Differential sensitivities of the prostacyclin and nitric oxide biosynthetic pathways to cytosolic calcium in bovine aortic endothelial cells
TLDR
Differences in Ca2+ ion sensitivity explain the selective inhibition of bradykinin‐stimulated PGI2 biosynthesis (to the exclusion of NO biosynthesis) by isoprenaline or forskolin, both of which attenuate brady Kinin‐dependent increases in [Ca2+]i.
Bioassay of an Endothelium-Derived Hyperpolarizing Factor from Bovine Coronary Arteries: Role of a Cytochrome P450 Metabolite
TLDR
The hypothesis that coronary arteries release an EDHF which is a cytochrome P450 metabolite of arachidonic acid is supported and stimulates the release of a transferable endothelial factor that activates KCa channels and hyperpolarizes coronary arterial smooth muscle cell membranes.
Characterization of endothelium‐derived hyperpolarizing factor as a cytochrome P450‐derived arachidonic acid metabolite in mammals.
TLDR
Investigation of the nature and mechanism of action of an as yet unidentified endothelium‐derived hyperpolarizing factor (EDHF) contributes to the dilator effect of bradykinin in different vascular beds finds that relaxations were significantly inhibited by the phospholipase A2 inhibitor, quinacrine, and the cytochrome P450 inhibitors.
Evidence against a cytochrome P450-derived reactive oxygen species as the mediator of the nitric oxide-independent vasodilator effect of bradykinin in the perfused heart of the rat.
TLDR
The coronary vasodilator action of BK is independent of superoxide or its derivatives, which can be excluded as hyperpolarizing factors mediating NO-independent vasodilation in the rat.
Human coronary arteriolar dilation to arachidonic acid depends on cytochrome P-450 monooxygenase and Ca2+-activated K+ channels.
TLDR
An important role is found for P450 metabolites in the regulation of human coronary arteriolar tone in the presence of endothelium-derived hyperpolarizing factors.
Pharmacologic Differentiation Between Endothelium‐Dependent Relaxations Sensitive and Resistant to Nitro‐L-Arginine in Coronary Arteries
TLDR
The results indicate that the bradykinin response is mediated by biosynthesis of EDRF, which is sensitive to L-NNA, and of EDHF, which are sensitive to TBA.
Nitric oxide and cGMP cause vasorelaxation by activation of a charybdotoxin-sensitive K channel by cGMP-dependent protein kinase.
TLDR
NO and cGMP relax vascular smooth muscle by a cG MP-dependent protein kinase-dependent activation of K channels, which suggests that the final common pathway shared by NO and the nitrovasodilators is cGmp-dependent K-channel activation.
...
...