ArticleBritish journal of pharmacology2000
An evaluation of potassium ions as endothelium-derived hyperpolarizing factor in porcine coronary 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 21 papers.
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Who cites it
21 citing papers in PubMed, 63 citations in OpenAlex.
- Pathophysiology and Outcomes of Endothelium Function in Coronary Microvascular Diseases: A Systematic Review of Randomized Controlled Trials and Multicenter Study.Biomedicines · 2022Review
- Initiation of migraine-related cortical spreading depolarization by hyperactivity of GABAergic neurons and NaV1.1 channels.The Journal of clinical investigation · 2021Article
- Role of connexins and pannexins in cardiovascular physiology.Cellular and molecular life sciences : CMLS · 2015Review
- Regulation of cellular communication by signaling microdomains in the blood vessel wall.Pharmacological reviews · 2014Review
- EDHF: spreading the influence of the endothelium.British journal of pharmacology · 2011Review
- The ATP-sensitive K(+)-channel (K(ATP)) controls early left-right patterning in Xenopus and chick embryos.Developmental biology · 2010Article
- Endothelium-derived hyperpolarising factors and associated pathways: a synopsis.Pflugers Archiv : European journal of physiology · 2010Review
- Physiological role of inward rectifier K(+) channels in vascular smooth muscle cells.Pflugers Archiv : European journal of physiology · 2008Review
- Crucial role of nitric oxide synthases system in endothelium-dependent hyperpolarization in mice.The Journal of experimental medicine · 2008Article
- Combination of Ca2+ -activated K+ channel blockers inhibits acetylcholine-evoked nitric oxide release in rat superior mesenteric artery.British journal of pharmacology · 2006Article
- Two distinct pathways account for EDHF-dependent dilatation in the gracilis artery of dyslipidaemic hApoB+/+ mice.British journal of pharmacology · 2005Article
- Loss of endothelial KATP channel-dependent, NO-mediated dilation of endocardial resistance coronary arteries in pigs with left ventricular hypertrophy.British journal of pharmacology · 2004Article
- Ouabain exerts biphasic effects on connexin functionality and expression in vascular smooth muscle cells.British journal of pharmacology · 2004Article
- Pivotal role of Cu,Zn-superoxide dismutase in endothelium-dependent hyperpolarization.The Journal of clinical investigation · 2003Article
- Ouabain exerts biphasic effects on connexin functionality and expression in vascular smooth muscle cells.British journal of pharmacology · 2003Article
- Evaluation of potassium ion as the endothelium-derived hyperpolarizing factor (EDHF) in the bovine coronary artery.British journal of pharmacology · 2003Article
- Acetylcholine-induced vasodilation may depend entirely upon NO in the femoral artery of young piglets.British journal of pharmacology · 2003Article
- Freshly isolated bovine coronary endothelial cells do not express the BK Ca channel gene.The Journal of physiology · 2002Article
- The Na-K-ATPase is a target for an EDHF displaying characteristics similar to potassium ions in the porcine renal interlobar artery.British journal of pharmacology · 2002Article
- Charybdotoxin-sensitive small conductance K(Ca) channel activated by bradykinin and substance P in endothelial cells.British journal of pharmacology · 2002Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the rat hepatic artery, the endothelium-derived hyperpolarizing factor (EDHF) was identified as potassium. Potassium hyperpolarizes the smooth muscles by gating inward rectified potassium channels and by activating the sodium-potassium adenosine triphosphatase (Na(+)-K(+)ATPase). Our goal was to examine whether potassium could explain the EDHF in porcine coronary arteries. On coronary strips, the inhibition of calcium-dependent potassium channels with 100 nM apamin plus 100 microM charibdotoxin inhibited the endothelium-dependent relaxations, produced by 10 nM substance P and 300 nM bradykinin and resistant to nitro-L-arginine and indomethacin. The scavenging of potassium with 2 mM Kryptofix 2.2.2 abolished the endothelium-dependent relaxations produced by the kinins and resistant to nitro-L-arginine and indomethacin. Forty microM 18alpha glycyrrethinic acid or 50 microM palmitoleic acid, both uncoupling agents, did not inhibit these kinin relaxations. Therefore, EDHF does not result from an electrotonic spreading of an endothelial hyperpolarization. Barium (0.3 nM) did not inhibit the kinin relaxations resistant to nitro-L-arginine and indomethacin. Therefore, EDHF does not result from the activation of inward rectified potassium channels. Five hundred nM ouabain abolished the endothelium-dependent relaxations resistant to nitro-L-arginine and indomethacin without inhibiting the endothelium-derived NO relaxation. The perifusion of a medium supplemented with potassium depolarized and contracted a coronary strip; however, the short application of potassium hyperpolarized the smooth muscles. These results are compatible with the concept that, in porcine coronary artery, the EDHF is potassium released by the endothelial cells and that this ion hyperpolarizes and relaxes the smooth muscles by activating the Na(+)-K(+)ATPase.
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