ArticleBritish journal of pharmacology2005
Two distinct pathways account for EDHF-dependent dilatation in the gracilis artery of dyslipidaemic hApoB+/+ mice.
Article in British journal of pharmacology, 2005. 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, 43 citations in OpenAlex.
- Endothelial function can be modulated by acute hyperglycemia.Scientific reports · 2025Article
- Studies on the Effects of Hypercholesterolemia on Mouse Ophthalmic Artery Reactivity.Diseases (Basel, Switzerland) · 2023Article
- Spironolactone treatment attenuates vascular dysfunction in type 2 diabetic mice by decreasing oxidative stress and restoring NO/GC signaling.Frontiers in physiology · 2015Article
- The anti-hypercholesterolemic effect of low p53 expression protects vascular endothelial function in mice.PloS one · 2014Article
- Postnatal exposure to voluntary exercise but not the antioxidant catechin protects the vasculature after a switch to an atherogenic environment in middle-age mice.Pflugers Archiv : European journal of physiology · 2013Article
- The biological effects of ivabradine in cardiovascular disease.Molecules (Basel, Switzerland) · 2012Review
- Enhanced K(+)-channel-mediated endothelium-dependent local and conducted dilation of small mesenteric arteries from ApoE(-/-) mice.Cardiovascular research · 2011Article
- Quick change artist: endothelium-derived relaxing factor in resistance arteries.Hypertension (Dallas, Tex. : 1979) · 2011Article
- Catechin treatment improves cerebrovascular flow-mediated dilation and learning abilities in atherosclerotic mice.American journal of physiology. Heart and circulatory physiology · 2011Article
- Endothelium-derived hyperpolarizing factor and diabetes.World journal of cardiology · 2011Article
- Endothelial dysfunction in diabetes: multiple targets for treatment.Pflugers Archiv : European journal of physiology · 2010Review
- Endothelial Ca+-activated K+ channels in normal and impaired EDHF-dilator responses--relevance to cardiovascular pathologies and drug discovery.British journal of pharmacology · 2009Review
- Calcium-activated potassium channels and endothelial dysfunction: therapeutic options?British journal of pharmacology · 2009Review
- Defying the economists: a decrease in heart rate improves not only cardiac but also endothelial function.British journal of pharmacology · 2008Article
- Chronic heart rate reduction by ivabradine prevents endothelial dysfunction in dyslipidaemic mice.British journal of pharmacology · 2008Article
- ROS-sensitive cytochrome P450 activity maintains endothelial dilatation in ageing but is transitory in dyslipidaemic mice.British journal of pharmacology · 2006Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
1 A universal endothelium-derived hyperpolarising factor (EDHF--non-NO/non-PGI(2)) has not been identified. EDHF, however, is essential for the physiological control of resistance artery tone. The impact of dyslipidaemia (DL), a risk factor for cardiovascular diseases, on the nature and the efficacy of EDHF has not been evaluated yet. 2 Pressurised (80 mmHg) gracilis arterial segments isolated from mice expressing the human apoB-100 and C57Bl/6 wild-type (WT) mice were used. EDHF-dependent dilatations to acetylcholine (ACh) were measured in the presence of L-NNA (100 microM, NOS inhibitor) and indomethacin (10 microM, COX inhibitor). 3 Maximal EDHF-induced dilatations were increased in DL when compared to WT (95+/-2 versus 86+/-4% in WT; P<0.05). Combination of apamin and charybdotoxin strongly reduced (P<0.05) ACh-induced dilatation in WT (22+/-4%) and DL (25+/-5%). 4 Combined addition of barium (Ba(2+)) and ouabain abolished EDHF-induced dilatations in WT arteries (13+/-3%; P<0.05). In vessels isolated from DL mice, however, only the addition of 14,15-EEZE (a 14,15-EET antagonist) to Ba(2+) and ouabain prevented EDHF-induced dilatations (5+/-3% compared to 54+/-11% in the presence of combined Ba(2+) and ouabain; P<0.05). 5 Our data suggest that EDHF-mediated dilatation depends on the opening of endothelial SK(Ca) and IK(Ca) channels. This is associated with the opening of K(ir) channels and activation of the Na(+)/K(+)-ATPase pump on smooth muscle cells leading to dilatation. In arteries from DL mice, a cytochrome P450 metabolite likely to be 14,15-EET equally contributes to the dilatory action of ACh. The early increased efficacy of EDHF in arteries isolated from DL mice may originate from the duplication of the EDHF pathways.
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