ArticleBritish journal of pharmacology2000
EDHF, NO and a prostanoid: hyperpolarization-dependent and -independent relaxation in guinea-pig arteries.
Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 55 citations in OpenAlex.
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- The Gatekeepers in the Mouse Ophthalmic Artery: Endothelium-Dependent Mechanisms of Cholinergic Vasodilation.Scientific reports · 2016Article
- Immunosuppressive/anti-inflammatory cytokines directly and indirectly inhibit endothelial dysfunction--a novel mechanism for maintaining vascular function.Journal of hematology & oncology · 2014Review
- Localization of relaxin receptors in arteries and veins, and region-specific increases in compliance and bradykinin-mediated relaxation after in vivo serelaxin treatment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Pulsed ultrasound enhances the delivery of nitric oxide from bubble liposomes to ex vivo porcine carotid tissue.International journal of nanomedicine · 2014Article
- Article
- Vitamin D insufficiency is associated with impaired vascular endothelial and smooth muscle function and hypertension in young rats.The Journal of physiology · 2011Article
- Uteroplacental insufficiency programs regional vascular dysfunction and alters arterial stiffness in female offspring.The Journal of physiology · 2010Article
- A role for nitroxyl (HNO) as an endothelium-derived relaxing and hyperpolarizing factor in resistance arteries.British journal of pharmacology · 2009Article
- Differential effects of nitric oxide synthase inhibitors on endothelium-dependent and nitrergic nerve-mediated vasodilatation in the bovine ciliary artery.British journal of pharmacology · 2007Article
- Intrauterine growth restriction delays cardiomyocyte maturation and alters coronary artery function in the fetal sheep.The Journal of physiology · 2007Article
- Disparity in osmolarity-induced vascular reactivity.Journal of the American Society of Nephrology : JASN · 2005Article
- Endothelium-dependent smooth muscle hyperpolarization: do gap junctions provide a unifying hypothesis?British journal of pharmacology · 2004Review
- Peritoneal dialysis solutions contract arteries through endothelium-independent prostanoid pathways.Advances in peritoneal dialysis. Conference on Peritoneal Dialysis · 2004Article
- Muscle contraction under capillaries in hamster muscle induces arteriolar dilatation via K(ATP) channels and nitric oxide.The Journal of physiology · 2002Article
- K+ currents underlying the action of endothelium-derived hyperpolarizing factor in guinea-pig, rat and human blood vessels.The Journal of physiology · 2001Article
- Role of EDHF in the vasodilatory effect of loop diuretics in guinea-pig mesenteric resistance arteries.British journal of pharmacology · 2000Article
- Vasoactive components of dialysis solution.Peritoneal dialysis international : journal of the International Society for Peritoneal DialysisArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The contribution of endothelium-derived hyperpolarizing factor (EDHF), nitric oxide (NO) and a prostanoid (PG) to endothelium-dependent hyperpolarization and relaxation were assessed in coronary and mammary arteries of guinea-pigs by integration of the responses evoked during discrete applications of acetylcholine (ACh). The results of this integration approach were compared with those using traditional peak analysis methods. N(omega)-nitro-L-arginine methyl ester (L-NAME, 100 microM) and indomethacin (1 microM), alone or in combination, were without effect on peak hyperpolarizations or relaxations while they markedly reduced the integrated responses in both arteries. Integrated responses attributed to NO and PG were larger than those attributed to EDHF in the coronary artery (at 2 microM ACh, hyperpolarization (mV s): NO, 4200+/-91; PG, 5046+/-157; EDHF, 1532+/-94; relaxation (mN s mm(-1)): NO, 2488+/-122; PG, 2234+/-96; EDHF, 802+/-54). Integrated responses attributed to NO, PG and EDHF were similar in the mammary artery (at 2 microM ACh, hyperpolarization: NO, 347+/-69; PG, 217+/-49; EDHF, 310+/-63; relaxation: NO, 462+/-94; PG, 456+/-144; EDHF, 458+/-40). Gilbenclamide (1 microM) all but abolished the hyperpolarization attributable to NO and PG but not EDHF in both arteries allowing assessment of the role of the hyperpolarization in relaxation. Gilbenclamide was without effect on the integrated relaxation due to NO but significantly reduced the relaxation associated with PG in the two arteries. In conclusion, integration of the responses enabled a more complete assessment of the contribution of EDHF, NO and PG to endothelium-dependent responses, which were strikingly different in the two arteries. There is commonality in the role of hyperpolarization in relaxation in both arteries: EDHF-dependent relaxation is strongly dependent on hyperpolarization; hyperpolarization plays an important role in PG relaxation, whereas it has a small facilitatory role in NO-dependent relaxation.
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