ArticleAmerican journal of physiology. Heart and circulatory physiology2010
Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Vasodilator reactive oxygen species ameliorate perturbed myocardial oxygen delivery in exercising swine with multiple comorbidities.Basic research in cardiology · 2024Article
- Expanding landscape of coronary microvascular disease in co-morbid conditions: Metabolic disease and beyond.Journal of molecular and cellular cardiology · 2024Review
- Supplementation with a Carob (Antioxidants (Basel, Switzerland) · 2020Article
- Article
- Reduced coronary reactive hyperemia in mice was reversed by the soluble epoxide hydrolase inhibitor (t-AUCB): Role of adenosine AProstaglandins & other lipid mediators · 2017Article
- Cardiovascular consequences of metabolic syndrome.Translational research : the journal of laboratory and clinical medicine · 2017Review
- Regulation of Coronary Blood Flow.Comprehensive Physiology · 2017Review
- Article
- Article
- Deletion of soluble epoxide hydrolase enhances coronary reactive hyperemia in isolated mouse heart: role of oxylipins and PPARγ.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Effect of Soluble Epoxide Hydrolase on the Modulation of Coronary Reactive Hyperemia: Role of Oxylipins and PPARγ.PloS one · 2016Article
- Impaired coronary collateral growth: miR-shaken neutrophils caught in the act.American journal of physiology. Heart and circulatory physiology · 2015Article
- Modeling cardiac arrest and resuscitation in the domestic pig.World journal of critical care medicine · 2015Review
- Contribution of hydrogen sulfide to the control of coronary blood flow.Microcirculation (New York, N.Y. : 1994) · 2014Article
- A1 adenosine receptor negatively modulates coronary reactive hyperemia via counteracting A2A-mediated H2O2 production and KATP opening in isolated mouse hearts.American journal of physiology. Heart and circulatory physiology · 2013Article
- Contribution of electromechanical coupling between Kv and Ca v1.2 channels to coronary dysfunction in obesity.Basic research in cardiology · 2013Article
- Exercise training-enhanced, endothelium-dependent dilation mediated by altered regulation of BK(Ca) channels in collateral-dependent porcine coronary arterioles.Microcirculation (New York, N.Y. : 1994) · 2013Article
- Large conductance, calcium- and voltage-gated potassium (BK) channels: regulation by cholesterol.Pharmacology & therapeutics · 2012Review
- Penitrem A as a tool for understanding the role of large conductance Ca(2+)/voltage-sensitive K(+) channels in vascular function.The Journal of pharmacology and experimental therapeutics · 2012Article
- Contribution of voltage-dependent K+ and Ca2+ channels to coronary pressure-flow autoregulation.Basic research in cardiology · 2012Article
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9 authors.
Funding
Abstract
This investigation tested the hypothesis that metabolic syndrome decreases the relative contribution of specific K(+) channels to coronary reactive hyperemia. Ca(2+)-activated (BK(Ca)), voltage-activated (K(V)), and ATP-dependent (K(ATP)) K(+) channels were investigated. Studies were conducted in anesthetized miniature Ossabaw swine fed a normal maintenance diet (11% kcal from fat) or an excess calorie atherogenic diet (43% kcal from fat, 2% cholesterol, 20% kcal from fructose) for 20 wk. The latter diet induces metabolic syndrome, increasing body weight, fasting glucose, total cholesterol, and triglyceride levels. Ischemic vasodilation was determined by the coronary flow response to a 15-s occlusion before and after cumulative administration of antagonists for BK(Ca) (penitrem A; 10 microg/kg iv), K(V) (4-aminopyridine; 0.3 mg/kg iv) and K(ATP) (glibenclamide; 1 mg/kg iv) channels. Coronary reactive hyperemia was diminished by metabolic syndrome as the repayment of flow debt was reduced approximately 30% compared with lean swine. Inhibition of BK(Ca) channels had no effect on reactive hyperemia in either lean or metabolic syndrome swine. Subsequent inhibition of K(V) channels significantly reduced the repayment of flow debt ( approximately 25%) in both lean and metabolic syndrome swine. Additional blockade of K(ATP) channels further diminished ( approximately 45%) the repayment of flow debt in lean but not metabolic syndrome swine. These data indicate that the metabolic syndrome impairs coronary vasodilation in response to cardiac ischemia via reductions in the contribution of K(+) channels to reactive hyperemia.
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