ArticleMicrovascular research2008
Influence of chronic alcohol consumption on inward rectifier potassium channels in cerebral arterioles.
Article in Microvascular research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 13 citations in OpenAlex.
- Alcohol and Hypertension-A Fresh Look on the Mechanistic Aspects of a Fatal Epidemiologic Relationship.Biomolecules · 2026Review
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Prenatal exposure to alcohol impairs responses of cerebral arterioles to activation of potassium channels: Role of oxidative stress.Alcohol, clinical & experimental research · 2023Article
- In vivo two-photon imaging of neuronal and brain vascular responses in mice chronically exposed to ethanol.Alcohol (Fayetteville, N.Y.) · 2020Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Effects of tempol and redox-cycling nitroxides in models of oxidative stress.Pharmacology & therapeutics · 2010Review
- Glutamate plasticity in the drunken amygdala: the making of an anxious synapse.International review of neurobiology · 2010Review
- Diabetes mellitus increases risk of vasospasm following aneurysmal subarachnoid hemorrhage independent of glycemic control.Neurocritical care · 2009Article
- The role of oxidative stress and NADPH oxidase in cerebrovascular disease.Trends in molecular medicine · 2008Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Inward rectifier potassium (K(IR)) channels appear to play an important role in the regulation of cerebral blood flow. Our goal was to examine the influence of chronic alcohol exposure on K(IR) channels in cerebral arterioles. Sprague-Dawley rats were fed liquid diets with or without alcohol for 8-12 weeks. Using intravital microscope, we measured diameter of pial arterioles in response to an inhibitor, BaCl(2), and an activator, KCl, of K(IR) channels in the absence and presence of a scavenger of reactive oxygen species, tempol, or an inhibitor of NAD(P)H oxidase, apocynin. Application of BaCl(2) (30 and 100 microM) produced dose-related vasoconstriction in non-alcohol-fed, but not in alcohol-fed rats. In addition, application of KCl (3, 10, and 30 mM) produced dose-related dilation in non-alcohol-fed and alcohol-fed rats, but the magnitude of vasodilatation was less in alcohol-fed rats. In contrast, nitroglycerin-induced vasodilation was similar in non-alcohol-fed and alcohol-fed rats. Superfusion of cranial window with tempol (0.1 mM) or apocynin (1 mM) did not alter baseline diameter and nitroglycerin-induced dilation of pial arterioles in non-alcohol-fed and alcohol-fed rats but significantly improved impaired KCl-induced dilation in alcohol-fed rats. Our findings suggest that chronic alcohol consumption impairs the role of K(IR) channels in basal tone and KCl-induced dilation of cerebral arterioles. In addition, impaired KCl-induced dilation of cerebral arterioles during alcohol consumption may be related to enhanced release of oxygen-derived free radicals via NAD(P)H oxidase.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.