ArticleJournal of molecular and cellular cardiology2012
Contribution of voltage-dependent K⁺ channels to metabolic control of coronary blood flow.
Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
47 citing papers in PubMed, 67 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- A new model of heart failure with preserved ejection fraction induced by metabolic syndrome in Ossabaw miniature swine.Basic research in cardiology · 2025Article
- Sexually dimorphic mechanisms of HJournal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- Myocardial oxygen handling and metabolic function of ex-situ perfused human hearts from circulatory death donors.JHLT open · 2024Article
- Impaired balance between coronary blood flow and myocardial metabolism in postpartum swine.Journal of molecular and cellular cardiology · 2024Article
- Expanding landscape of coronary microvascular disease in co-morbid conditions: Metabolic disease and beyond.Journal of molecular and cellular cardiology · 2024Review
- Unraveling the Gordian knot of coronary pressure-flow autoregulation.Journal of molecular and cellular cardiology · 2024Review
- Lung transcriptomics reveals the underlying mechanism by which aerobic training enhances pulmonary function in chronic obstructive pulmonary disease.BMC pulmonary medicine · 2024Article
- Effect of Hydrogen Sulfide on Sympathoinhibition in Obese Pithed Rats and Participation of KInternational journal of hypertension · 2024Article
- Takotsubo syndrome is a coronary microvascular disease: experimental evidence.European heart journal · 2023Article
- Exercise training rescues impaired HAmerican journal of physiology. Heart and circulatory physiology · 2023Article
- Chronic high-rate pacing induces heart failure with preserved ejection fraction-like phenotype in Ossabaw swine.Basic research in cardiology · 2022Article
- Multiscale model of the physiological control of myocardial perfusion to delineate putative metabolic feedback mechanisms.The Journal of physiology · 2022Article
- Functional and structural adaptations of the coronary macro- and microvasculature to regular aerobic exercise by activation of physiological, cellular, and molecular mechanisms: ESC Working Group on Coronary Pathophysiology and Microcirculation position paper.Cardiovascular research · 2022Review
- Mineralocorticoid receptor blockade normalizes coronary resistance in obese swine independent of functional alterations in KBasic research in cardiology · 2021Article
- Guidelines for animal exercise and training protocols for cardiovascular studies.American journal of physiology. Heart and circulatory physiology · 2020Review
- Experimental animal models of coronary microvascular dysfunction.Cardiovascular research · 2020Review
- Disentangling the Gordian knot of local metabolic control of coronary blood flow.American journal of physiology. Heart and circulatory physiology · 2020Review
- KMicrocirculation (New York, N.Y. : 1994) · 2018Review
- KMicrocirculation (New York, N.Y. : 1994) · 2018Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The purpose of this investigation was to test the hypothesis that K(V) channels contribute to metabolic control of coronary blood flow and that decreases in K(V) channel function and/or expression significantly attenuate myocardial oxygen supply-demand balance in the metabolic syndrome (MetS). Experiments were conducted in conscious, chronically instrumented Ossabaw swine fed either a normal maintenance diet or an excess calorie atherogenic diet that produces the clinical phenotype of early MetS. Data were obtained under resting conditions and during graded treadmill exercise before and after inhibition of K(V) channels with 4-aminopyridine (4-AP, 0.3mg/kg, iv). In lean-control swine, 4-AP reduced coronary blood flow ~15% at rest and ~20% during exercise. Inhibition of K(V) channels also increased aortic pressure (P<0.01) while reducing coronary venous PO(2) (P<0.01) at a given level of myocardial oxygen consumption (MVO(2)). Administration of 4-AP had no effect on coronary blood flow, aortic pressure, or coronary venous PO(2) in swine with MetS. The lack of response to 4-AP in MetS swine was associated with a ~20% reduction in coronary K(V) current (P<0.01) and decreased expression of K(V)1.5 channels in coronary arteries (P<0.01). Together, these data demonstrate that K(V) channels play an important role in balancing myocardial oxygen delivery with metabolism at rest and during exercise-induced increases in MVO(2). Our findings also indicate that decreases in K(V) channel current and expression contribute to impaired control of coronary blood flow in the MetS. This article is part of a Special Issue entitled "Coronary Blood Flow".
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Registered trials
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