ArticleCirculation research2015
Requisite Role of Kv1.5 Channels in Coronary Metabolic Dilation.
Article in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 97 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
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- Human adaptation response to obesity.International journal of obesity (2005) · 2025Review
- Ubiquitination is involved in PKC-mediated degradation of cell surface Kv1.5 channels.The Journal of biological chemistry · 2024Article
- Unraveling the Gordian knot of coronary pressure-flow autoregulation.Journal of molecular and cellular cardiology · 2024Review
- Kv beta complex facilitates exercise-induced augmentation of myocardial perfusion and cardiac growth.Frontiers in cardiovascular medicine · 2024Article
- Inhibitory effects of N-methyl-D-aspartate (NMDA) and αNaunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Role of miR-204 in segmental cardiac effects of phenylephrine and pressure overload.Biochemical and biophysical research communications · 2023Article
- Basal NAD(H) redox state permits hydrogen peroxide-induced mesenteric artery dilatation.The Journal of physiology · 2023Article
- Takotsubo syndrome is a coronary microvascular disease: experimental evidence.European heart journal · 2023Article
- Myocardial Infarction with Non-Obstructive Coronary Arteries (MINOCA): Focus on Coronary Microvascular Dysfunction and Genetic Susceptibility.Journal of clinical medicine · 2023Review
- Exercise training rescues impaired HAmerican journal of physiology. Heart and circulatory physiology · 2023Article
- Protection against Ischemic Heart Disease: A Joint Role for eNOS and the KInternational journal of molecular sciences · 2023Article
- Deletion of Smooth Muscle O-GlcNAc Transferase Prevents Development of Atherosclerosis in Western Diet-Fed Hyperglycemic ApoEInternational journal of molecular sciences · 2023Article
- Review
- Pyridine nucleotide redox potential in coronary smooth muscle couples myocardial blood flow to cardiac metabolism.Nature communications · 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
- Cellular Prion Protein Is Essential for Myocardial Regeneration but Not the Recovery of Left Ventricular Function from Apical Ballooning.Biomedicines · 2022Article
- KCurrent topics in membranes · 2022Review
- Alcohol Use Disorders and Their Harmful Effects on the Contractility of Skeletal, Cardiac and Smooth Muscles.Advances in drug and alcohol research · 2021Article
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Authors and funding
20 authors at 1 institution in 1 country.
Funding
Abstract
rationaleIn the working heart, coronary blood flow is linked to the production of metabolites, which modulate tone of smooth muscle in a redox-dependent manner. Voltage-gated potassium channels (Kv), which play a role in controlling membrane potential in vascular smooth muscle, have certain members that are redox-sensitive.
objectiveTo determine the role of redox-sensitive Kv1.5 channels in coronary metabolic flow regulation. METHODS AND
resultsIn mice (wild-type [WT], Kv1.5 null [Kv1.5(-/-)], and Kv1.5(-/-) and WT with inducible, smooth muscle-specific expression of Kv1.5 channels), we measured mean arterial pressure, myocardial blood flow, myocardial tissue oxygen tension, and ejection fraction before and after inducing cardiac stress with norepinephrine. Cardiac work was estimated as the product of mean arterial pressure and heart rate. Isolated arteries were studied to establish whether genetic alterations modified vascular reactivity. Despite higher levels of cardiac work in the Kv1.5(-/-) mice (versus WT mice at baseline and all doses of norepinephrine), myocardial blood flow was lower in Kv1.5(-/-) mice than in WT mice. At high levels of cardiac work, tissue oxygen tension dropped significantly along with ejection fraction. Expression of Kv1.5 channels in smooth muscle in the null background rescued this phenotype of impaired metabolic dilation. In isolated vessels from Kv1.5(-/-) mice, relaxation to H2O2 was impaired, but responses to adenosine and acetylcholine were normal compared with those from WT mice.
conclusionsKv1.5 channels in vascular smooth muscle play a critical role in coupling myocardial blood flow to cardiac metabolism. Absence of these channels disassociates metabolism from flow, resulting in cardiac pump dysfunction and tissue hypoxia.
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