ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Fundamental increase in pressure-dependent constriction of brain parenchymal arterioles from subarachnoid hemorrhage model rats due to membrane depolarization.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 80 citations in OpenAlex.
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- Protein kinase Cδ and pharmacomechanical coupling: Re-envisioning cerebral vascular control.The Journal of physiology · 2026Article
- Systems biology analysis of vasodynamics in mouse cerebral arterioles during resting state and functional hyperemia.PLoS computational biology · 2026Article
- Pathophysiological mechanisms underlying early brain injury and delayed cerebral ischemia in the aftermath of aneurysmal subarachnoid hemorrhage: a comprehensive analysis.Frontiers in neurology · 2025Review
- Increased triglyceride-glucose index is associated with adverse functional outcome for patients with aneurysmal subarachnoid hemorrhage after surgical clipping and endovascular coiling: insights from a large cohort study.Frontiers in neurology · 2025Article
- Vascular Function and Ion Channels in Alzheimer's Disease.Microcirculation (New York, N.Y. : 1994) · 2024Review
- Distinct potassium channel types in brain capillary pericytes.Biophysical journal · 2024Article
- Nitric oxide synthase and reduced arterial tone contribute to arteriovenous malformation.Science advances · 2023Article
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- Intraluminal pressure elevates intracellular calcium and contracts CNS pericytes: Role of voltage-dependent calcium channels.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
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- Pyridine nucleotide redox potential in coronary smooth muscle couples myocardial blood flow to cardiac metabolism.Nature communications · 2022Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- The Calcium Signaling Mechanisms in Arterial Smooth Muscle and Endothelial Cells.Comprehensive Physiology · 2021Article
- Myocardial Blood Flow Control by Oxygen Sensing Vascular Kvβ Proteins.Circulation research · 2021Article
- Impaired Cerebral Autoregulation After Subarachnoid Hemorrhage: A Quantitative Assessment Using a Mouse Model.Frontiers in physiology · 2021Article
- Secondhand Smoke Exposure Impairs Ion Channel Function and Contractility of Mesenteric Arteries.Function (Oxford, England) · 2021Article
- Cerebral Autoregulation in Subarachnoid Hemorrhage.Frontiers in neurology · 2021Review
- Ex Vivo Pressurized Hippocampal Capillary-Parenchymal Arteriole Preparation for Functional Study.Journal of visualized experiments : JoVE · 2019Article
- Tonic regulation of middle meningeal artery diameter by ATP-sensitive potassium channels.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Intracerebral (parenchymal) arterioles are morphologically and physiologically unique compared with pial arteries and arterioles. The ability of subarachnoid hemorrhage (SAH) to induce vasospasm in large-diameter pial arteries has been extensively studied, although the contribution of this phenomenon to patient outcome is controversial. Currently, little is known regarding the impact of SAH on parenchymal arterioles, which are critical for regulation of local and global cerebral blood flow. Here diameter, smooth muscle intracellular Ca(2+) concentration ([Ca(2+)](i)), and membrane potential measurements were used to assess the function of intact brain parenchymal arterioles isolated from unoperated (control), sham-operated, and SAH model rats. At low intravascular pressure (5 mmHg), membrane potential and [Ca(2+)](i) were not different in arterioles from control, sham-operated, and SAH animals. However, raising intravascular pressure caused significantly greater membrane potential depolarization, elevation in [Ca(2+)](i), and constriction in SAH arterioles. This SAH-induced increase in [Ca(2+)](i) and tone occurred in the absence of the vascular endothelium and was abolished by the L-type voltage-dependent calcium channel (VDCC) inhibitor nimodipine. Arteriolar [Ca(2+)](i) and tone were not different between groups when smooth muscle membrane potential was adjusted to the same value. Protein and mRNA levels of the L-type VDCC Ca(V)1.2 were similar in parenchymal arterioles isolated from control and SAH animals, suggesting that SAH did not cause VDCC upregulation. We conclude that enhanced parenchymal arteriolar tone after SAH is driven by smooth muscle membrane potential depolarization, leading to increased L-type VDCC-mediated Ca(2+) influx.
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