ArticleCirculation research2012
Acidosis dilates brain parenchymal arterioles by conversion of calcium waves to sparks to activate BK channels.
Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 111 citations in OpenAlex.
- Acid-sensing ion channels as sensors of brain metabolic state.Pflugers Archiv : European journal of physiology · 2026Review
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- Systems biology analysis of vasodynamics in mouse cerebral arterioles during resting state and functional hyperemia.PLoS computational biology · 2026Article
- Persistent dysmorphology and dysfunction of the brain microvasculature following repeated trauma.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Article
- Cooling down for going up: Could selective 'brain chilling' mitigate high-altitude illness?Experimental physiology · 2025Article
- Fetal Cerebral Blood Flow (Dys)autoregulation.Diagnostics (Basel, Switzerland) · 2025Review
- Obesity-Associated Adiposomes Promote Vascular Smooth Muscle Cell Hypercontractility.Comprehensive Physiology · 2025Article
- Estrogen Enhances SK Channel Activity to Limit Hippocampal Arteriole Constriction.Circulation research · 2025Article
- Characterizing the protective vasodilatory effects of hypobaric hypoxia on the neurovascular coupling response.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Article
- High-fat feeding has sex-dependent effects on the structure and biomechanical properties of cerebral parenchymal arterioles and cognitive function.American journal of physiology. Heart and circulatory physiology · 2025Article
- The pathogenesis of cerebral small vessel disease and vascular cognitive impairment.Physiological reviews · 2025Review
- Fluorescent sensors for intracellular signaling in the brain: imaging neurons, glia, and vascular cells.Neurophotonics · 2025Article
- Increased luminal pressure in brain capillaries drives TRPC3-dependent depolarization and constriction of transitional pericytes.Science signaling · 2025Article
- KProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Vascular Function and Ion Channels in Alzheimer's Disease.Microcirculation (New York, N.Y. : 1994) · 2024Review
- Neurovascular coupling and CONature communications · 2024Article
- Mitochondrial Ca2+-coupled generation of reactive oxygen species, peroxynitrite formation, and endothelial dysfunction in Cantú syndrome.JCI insight · 2024Article
- Spreading depolarizations pose critical energy challenges in acute brain injury.Journal of neurochemistry · 2024Review
- Deviation From Personalized Blood Pressure Targets Correlates With Worse Outcome After Successful Recanalization.Journal of the American Heart Association · 2024Article
21 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
rationaleAcidosis is a powerful vasodilator signal in the brain circulation. However, the mechanisms by which this response occurs are not well understood, particularly in the cerebral microcirculation. One important mechanism to dilate cerebral (pial) arteries is by activation of large-conductance, calcium-sensitive potassium (BK(Ca)) channels by local Ca(2+) signals (Ca(2+) sparks) through ryanodine receptors (RyRs). However, the role of this pathway in the brain microcirculation is not known.
objectiveThe objectives of this study were to determine the mechanism by which acidosis dilates brain parenchymal arterioles (PAs) and to elucidate the roles of RyRs and BK(Ca) channels in this response. METHODS AND
resultsInternal diameter and vascular smooth muscle cell Ca(2+) signals were measured in isolated pressurized murine PAs, using imaging techniques. In physiological pH (7.4), vascular smooth muscle cells exhibited primarily RyR-dependent Ca(2+) waves. Reducing external pH from 7.4 to 7.0 in both normocapnic and hypercapnic conditions decreased Ca(2+) wave activity, and dramatically increased Ca(2+) spark activity. Acidic pH caused a dilation of PAs which was inhibited by about 60% by BK(Ca) channel or RyR blockers, in a nonadditive manner. Similarly, dilator responses to acidosis were reduced by nearly 60% in arterioles from BK(Ca) channel knockout mice. Dilations induced by acidic pH were unaltered by inhibitors of K(ATP) channels or nitric oxide synthase.
conclusionsThese results support the novel concept that acidification, by converting Ca(2+) waves to sparks, leads to the activation of BK(Ca) channels to induce dilation of cerebral PAs.
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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.