ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2009
Impaired mitochondria-dependent vasodilation in cerebral arteries of Zucker obese rats with insulin resistance.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- Cyclooxygenase-derived vasoconstriction restrains hypoxia-mediated cerebral vasodilation in young adults with metabolic syndrome.American journal of physiology. Heart and circulatory physiology · 2014Trial
- The role of telomerase reverse transcriptase in the mitochondrial protective functions of Angiotensin-(1-7) in diabetic CD34Biochemical pharmacology · 2024Article
- Cardiometabolic health, menopausal estrogen therapy and the brain: How effects of estrogens diverge in healthy and unhealthy preclinical models of aging.Frontiers in neuroendocrinology · 2023Review
- Neuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome. A translational perspective.Frontiers in neuroscience · 2023Review
- Effects of prolonged type 2 diabetes on mitochondrial function in cerebral blood vessels.American journal of physiology. Heart and circulatory physiology · 2019Article
- Mitochondrial depolarization stimulates vascular repair-relevant functions of CD34British journal of pharmacology · 2019Article
- Fetal Cerebral Artery Mitochondrion as Target of Prenatal Alcohol Exposure.International journal of environmental research and public health · 2019Review
- Endothelium-dependent relaxation induced by etomidate in the aortas of insulin-resistant rats.Archives of medical science : AMS · 2018Article
- Impact of Metabolic Diseases on Cerebral Circulation: Structural and Functional Consequences.Comprehensive Physiology · 2018Review
- The Role of Endothelial CaInternational journal of molecular sciences · 2018Review
- Impaired Mitochondrial Respiration in Large Cerebral Arteries of Rats with Type 2 Diabetes.Journal of vascular research · 2017Article
- Role of Mitochondria in Cerebral Vascular Function: Energy Production, Cellular Protection, and Regulation of Vascular Tone.Comprehensive Physiology · 2016Review
- Depolarization of mitochondria in neurons promotes activation of nitric oxide synthase and generation of nitric oxide.American journal of physiology. Heart and circulatory physiology · 2016Article
- The mitochondrial function of the cerebral vasculature in insulin-resistant Zucker obese rats.American journal of physiology. Heart and circulatory physiology · 2016Article
- H2S- and NO-Signaling Pathways in Alzheimer's Amyloid Vasculopathy: Synergism or Antagonism?Frontiers in physiology · 2015Review
- Sustained mitochondrial functioning in cerebral arteries after transient ischemic stress in the rat: a potential target for therapies.American journal of physiology. Heart and circulatory physiology · 2014Article
- Diversity of mitochondria-dependent dilator mechanisms in vascular smooth muscle of cerebral arteries from normal and insulin-resistant rats.American journal of physiology. Heart and circulatory physiology · 2014Article
- The effects of obesity on the cerebral vasculature.Current vascular pharmacology · 2014Review
- Mitochondrial mechanisms in cerebral vascular control: shared signaling pathways with preconditioning.Journal of vascular research · 2014Review
- Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitochondria affect cerebrovascular tone by activation of mitochondrial ATP-sensitive K+ (K ATP) channels and generation of reactive oxygen species (ROS). Insulin resistance accompanying obesity causes mitochondrial dysfunction, but the consequences on the cerebral circulation have not been fully identified. We evaluated the mitochondrial effects of diazoxide, a putative mitochondrial K ATP channel activator, on cerebral arteries of Zucker obese (ZO) rats with insulin resistance and lean (ZL) controls. Diameter measurements showed diminished diazoxide-induced vasodilation in ZO compared with ZL rats. Maximal relaxation was 38 +/- 3% in ZL vs. 21 +/- 4% in ZO rats (P < 0.05). Iberiotoxin, a Ca2+-activated K+ channel inhibitor, or manganese(III) tetrakis(4-benzoic acid)porphyrin chloride, an SOD mimetic, or endothelial denudation diminished vasodilation to diazoxide, implicating Ca2+-activated K+ channels, ROS, and endothelial factors in vasodilation. Inhibition of nitric oxide synthase (NOS) in ZL rats diminished diazoxide-induced vasodilation in intact arteries, but vasodilation was unaffected in endothelium-denuded arteries. In contrast, NOS inhibition in ZO rats enhanced vasodilation in endothelium-denuded arteries, but intact arteries were unaffected, suggesting that activity of endothelial NOS was abolished, whereas factors derived from nonendothelial NOS promoted vasoconstriction. Fluorescence microscopy showed decreased mitochondrial depolarization, ROS production, and nitric oxide generation in response to diazoxide in ZO arteries. Protein and mRNA measurements revealed increased expression of endothelial NOS and SODs in ZO arteries. Thus, cerebrovascular dilation to mitochondria-derived factors involves integration of endothelial and smooth muscle mechanisms. Furthermore, mitochondria-mediated vasodilation was diminished in ZO rats due to impaired mitochondrial K(ATP) channel activation, diminished mitochondrial ROS generation, increased ROS scavenging, and abnormal NOS activity.
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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.