ArticleBritish journal of pharmacology2000
Role of gap junctions and EETs in endothelium-dependent hyperpolarization of porcine coronary artery.
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 33 papers.
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Who cites it
33 citing papers in PubMed.
- Pathophysiology and Outcomes of Endothelium Function in Coronary Microvascular Diseases: A Systematic Review of Randomized Controlled Trials and Multicenter Study.Biomedicines · 2022Review
- Differential hyperpolarization to substance P and calcitonin gene-related peptide in smooth muscle versus endothelium of mouse mesenteric artery.Microcirculation (New York, N.Y. : 1994) · 2021Article
- Functional Tuning of Intrinsic Endothelial Ca2+ Dynamics in Swine Coronary Arteries.Circulation research · 2016Article
- The role of epoxyeicosatrienoic acids in the cardiovascular system.British journal of clinical pharmacology · 2015Review
- Age-related impairment of conducted dilation in human coronary arterioles.American journal of physiology. Heart and circulatory physiology · 2014Article
- Sex differences in endothelial function in porcine coronary arteries: a role for H2O2 and gap junctions?British journal of pharmacology · 2014Article
- Endothelial control of vasodilation: integration of myoendothelial microdomain signalling and modulation by epoxyeicosatrienoic acids.Pflugers Archiv : European journal of physiology · 2014Review
- KV 7 channels are involved in hypoxia-induced vasodilatation of porcine coronary arteries.British journal of pharmacology · 2014Article
- Reactive oxygen species and the cardiovascular system.Oxidative medicine and cellular longevity · 2013Review
- Impaired vasodilation in the pathogenesis of hypertension: focus on nitric oxide, endothelial-derived hyperpolarizing factors, and prostaglandins.Journal of clinical hypertension (Greenwich, Conn.) · 2012Review
- Microvascular responsiveness in obesity: implications for therapeutic intervention.British journal of pharmacology · 2012Review
- EDHF: spreading the influence of the endothelium.British journal of pharmacology · 2011Review
- Endothelium-derived hyperpolarizing factor in the brain: influence of sex, vessel size and disease state.Women's health (London, England) · 2011Article
- Connexins and gap junctions in the EDHF phenomenon and conducted vasomotor responses.Pflugers Archiv : European journal of physiology · 2010Review
- Endothelium-derived hyperpolarising factors and associated pathways: a synopsis.Pflugers Archiv : European journal of physiology · 2010Review
- Openers of calcium-activated potassium channels and endothelium-dependent hyperpolarizations in the guinea pig carotid artery.Naunyn-Schmiedeberg's archives of pharmacology · 2008Article
- KIR channels function as electrical amplifiers in rat vascular smooth muscle.The Journal of physiology · 2008Article
- Bradykinin-induced, endothelium-dependent responses in porcine coronary arteries: involvement of potassium channel activation and epoxyeicosatrienoic acids.British journal of pharmacology · 2005Article
- Role of SK(Ca) and IK(Ca) in endothelium-dependent hyperpolarizations of the guinea-pig isolated carotid artery.British journal of pharmacology · 2005Article
- Connexin-mimetic peptides dissociate electrotonic EDHF-type signalling via myoendothelial and smooth muscle gap junctions in the rabbit iliac artery.British journal of pharmacology · 2005Article
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Authors and funding
7 authors.
Funding
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Abstract
1. The effects of endothelium-derived hyperpolarizing factor (EDHF: elicited using substance P or bradykinin) were compared with those of 11,12-EET in pig coronary artery. Smooth muscle cells were usually impaled with microelectrodes through the adventitial surface. 2. Substance P (100 nM) and 11,12-EET (11,12-epoxyeicosatrienoic acid; 3 microM) hyperpolarized endothelial cells in intact arteries. These actions were unaffected by 100 nM iberiotoxin but were abolished by charybdotoxin plus apamin (each 100 nM). 3. Substance P (100 nM) and bradykinin (30 nM) hyperpolarized intact artery smooth muscle; Substance P had no effect after endothelium removal. 11,12-EET hyperpolarized de-endothelialized vessels by 12.6+/-0.3 mV, an effect abolished by 100 nM iberiotoxin. 4. 11,12-EET hyperpolarized intact arteries by 18.6+/-0.8 mV, an action reduced by iberiotoxin, which was ineffective against substance P. Hyperpolarizations to 11, 12-EET and substance P were partially inhibited by 100 nM charybdotoxin and abolished by further addition of 100 nM apamin. 5. 30 microM barium plus 500 nM ouabain depolarized intact artery smooth muscle but responses to substance P and bradykinin were unchanged. 500 microM gap 27 markedly reduced hyperpolarizations to substance P and bradykinin which were abolished in the additional presence of barium plus ouabain. 6. Substance P-induced hyperpolarizations of smooth muscle cells immediately below the internal elastic lamina were unaffected by gap 27, even in the presence of barium plus ouabain. 7. In pig coronary artery, 11,12-EET is not EDHF. Smooth muscle hyperpolarizations attributed to 'EDHF' are initiated by endothelial cell hyperpolarization involving charybdotoxin- (but not iberiotoxin) and apamin-sensitive K(+) channels. This may spread electrotonically via myoendothelial gap junctions but the involvement of an unknown endothelial factor cannot be excluded.
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