ArticleThe Journal of physiology2002
Role for endothelium-derived hyperpolarizing factor in vascular tone in rat mesenteric and hindlimb circulations in vivo.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 70 citations in OpenAlex.
- Article
- 17β-Estradiol Treatment Improves Acetylcholine-Induced Relaxation of Mesenteric Arteries in Ovariectomized UC Davis Type 2 Diabetes Mellitus Rats in Prediabetic State.Frontiers in physiology · 2022Article
- Potentiation of Acetylcholine-Induced Relaxation of Aorta in Male UC Davis Type 2 Diabetes Mellitus (UCD-T2DM) Rats: Sex-Specific Responses.Frontiers in physiology · 2021Article
- Age-dependent impact of CaThe Journal of physiology · 2016Article
- Article
- Exercise training augments neuronal nitric oxide synthase-mediated inhibition of sympathetic vasoconstriction in contracting skeletal muscle of rats.The Journal of physiology · 2014Article
- Sex differences in mesenteric endothelial function of streptozotocin-induced diabetic rats: a shift in the relative importance of EDRFs.American journal of physiology. Heart and circulatory physiology · 2012Article
- Dynamic Ca(2+) signal modalities in the vascular endothelium.Microcirculation (New York, N.Y. : 1994) · 2012Review
- Novel role of endothelial BKCa channels in altered vasoreactivity following hypoxia.American journal of physiology. Heart and circulatory physiology · 2010Article
- Recycling of the Ca2+-activated K+ channel, KCa2.3, is dependent upon RME-1, Rab35/EPI64C, and an N-terminal domain.The Journal of biological chemistry · 2010Article
- Genetic ablation of calcium-independent phospholipase A(2)beta causes hypercontractility and markedly attenuates endothelium-dependent relaxation to acetylcholine.American journal of physiology. Heart and circulatory physiology · 2010Article
- Vascular pharmacology of epoxyeicosatrienoic acids.Advances in pharmacology (San Diego, Calif.) · 2010Review
- Calcium-activated potassium channels and endothelial dysfunction: therapeutic options?British journal of pharmacology · 2009Review
- Endothelium-derived hyperpolarizing factor as an in vivo back-up mechanism in the cutaneous microcirculation in old mice.The Journal of physiology · 2007Article
- Dietary soy modulates endothelium-dependent relaxation in aged male rats: Increased agonist-induced endothelium-derived hyperpolarising factor and basal nitric oxide activity.Free radical biology & medicine · 2006Article
- Thromboxane receptor stimulation associated with loss of SKCa activity and reduced EDHF responses in the rat isolated mesenteric artery.British journal of pharmacology · 2004Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of endothelium-derived hyperpolarizing factor (EDHF) in the regulation of blood flow in vivo was examined in the mesenteric and hindlimb circulations of anaesthetized rats. Basal mesenteric conductance decreased from 57 +/- 5 to 20 +/- 6 microl min(-1) mmHg(-1) when nitric oxide (NO) production was inhibited, and combined blockade of intermediate- and small-conductance Ca(2+)-activated K(+) (K(Ca)) channels with charybdotoxin (ChTx) and apamin had no further effect. Basal hindlimb conductance was reduced from 39 +/- 3 to 22 +/- 2 microl min(-1) mmHg(-1) by NO synthesis inhibition, with no effect of the K(Ca) channel blockers. Endothelial stimulation with acetylcholine (ACh) infusion directly into the mesenteric bed increased conductance by 20 +/- 2 microl min(-1) mmHg(-1). Blockade of NO synthesis decreased this conductance to 15 +/- 1 microl min(-1) mmHg(-1), leaving the response attributable to EDHF. This was reduced to 2 +/- 1 microl min(-1) mmHg(-1) by ChTx plus apamin but not by iberiotoxin, which selectively blocks large-conductance K(Ca) channels. Similar results were obtained when bradykinin (BK) was used to stimulate the endothelium. Nitroprusside, which directly relaxes smooth muscle, evoked an increase in conductance that was resistant to all blockers tested. ACh-induced increases in hindlimb conductance were reduced from 19 +/- 1 to 12 +/- 1 microl min(-1) mmHg(-1) by NO synthesis inhibition and further reduced to 2 +/- 2 microl min(-1) mmHg(-1) by ChTx plus apamin. In contrast to NO, ChTx- and apamin-sensitive EDHF appears to contribute little to basal conductance in rat mesenteric and hindlimb beds. However, EDHF accounts for a significant component of the conductance increase during endothelial stimulation by ACh and BK. In these beds, intermediate- and small-conductance K(Ca) channels underpin EDHF-mediated vasodilatation.
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