ArticleJournal of applied physiology (Bethesda, Md. : 1985)2009
Effects of chronic hypoxia on soluble guanylate cyclase activity in fetal and adult ovine cerebral arteries.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Involvement of Melatonin, Oxidative Stress, and Inflammation in the Protective Mechanism of the Carotid Artery over the Torpor-Arousal Cycle of Ground Squirrels.International journal of molecular sciences · 2024Article
- Cardiovascular responses to mild perinatal asphyxia in growth-restricted preterm lambs.American journal of physiology. Heart and circulatory physiology · 2023Article
- Maternal Undernutrition Modulates Neonatal Rat Cerebrovascular Structure, Function, and Vulnerability to Mild Hypoxic-Ischemic Injury via Corticosteroid-Dependent and -Independent Mechanisms.International journal of molecular sciences · 2021Article
- Prenatal metyrapone treatment modulates neonatal cerebrovascular structure, function, and vulnerability to mild hypoxic-ischemic injury.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Fetal Cerebrovascular Maturation: Effects of Hypoxia.Seminars in pediatric neurology · 2018Review
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- The fetal cerebral circulation: three decades of exploration by the LLU Center for Perinatal Biology.Advances in experimental medicine and biology · 2014Article
- Vasotrophic regulation of age-dependent hypoxic cerebrovascular remodeling.Current vascular pharmacology · 2013Review
- Cerebral artery signal transduction mechanisms: developmental changes in dynamics and Ca2+ sensitivity.Current vascular pharmacology · 2013Review
- Chronic hypoxia and VEGF differentially modulate abundance and organization of myosin heavy chain isoforms in fetal and adult ovine arteries.American journal of physiology. Cell physiology · 2012Article
- Hypoxic regulation of pulmonary vascular smooth muscle cyclic guanosine monophosphate-dependent kinase by the ubiquitin conjugating system.American journal of respiratory cell and molecular biology · 2012Article
- Fetal cerebral oxygenation: the homeostatic role of vascular adaptations to hypoxic stress.Advances in experimental medicine and biology · 2011Article
- cGMP-dependent protein kinases and cGMP phosphodiesterases in nitric oxide and cGMP action.Pharmacological reviews · 2010Review
- Nitric oxide/cGMP signalling induces Escherichia coli K1 receptor expression and modulates the permeability in human brain endothelial cell monolayers during invasion.Cellular microbiology · 2010Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
A broad variety of evidence obtained largely in pulmonary vasculature suggests that chronic hypoxia modulates vasoreactivity to nitric oxide (NO). The present study explores the general hypothesis that chronic hypoxia also modulates cerebrovascular reactivity to NO, and does so by modulating the activity of soluble guanylate cyclase (sGC), the primary target for NO in vascular smooth muscle. Pregnant and nonpregnant ewes were maintained at either sea level or at 3,820 m for the final 110 days of gestation, at which time middle cerebral arteries from term fetal lambs and nonpregnant adults were harvested. In both fetal and adult arteries, NO-induced vasodilatation was attenuated by chronic hypoxia and completely inhibited by 10 microM 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), a selective inhibitor of sGC. sGC abundance (in ng sGC/mg protein) measured via Western immunoblots was approximately 10-fold greater in fetal (17.6 +/- 1.6) than adult (1.7 +/- 0.3) arteries but was not affected by chronic hypoxia. The specific activity of sGC (in pmol cGMP.microg sGC(-1).min(-1)) was similar in fetal (255 +/- 64) and adult (280 +/- 75) arteries and was inhibited by chronic hypoxia in both fetal (120 +/- 10) and adult (132 +/- 26) arteries. Rates of cGMP degradation (in pmol cGMP.mg protein(-1).min(-1)) were similar in fetal (159 +/- 59) and adult (134 +/- 36) arteries but were not significantly depressed by chronic hypoxia in either fetal (115 +/- 25) or adult (108 +/- 25) arteries. The cGMP analog 8-(p-chlorophenylthio)-cGMP was a more potent vasorelaxant in fetal (pD(2) = 4.7 +/- 0.1) than adult (pD(2) = 4.3 +/- 0.1) arteries, but its ability to promote vasodilatation was not affected by chronic hypoxia in either age group. Together, these results reveal that hypoxic inhibition of NO-induced vasodilatation is attributable largely to attenuation of the specific activity of sGC and does not involve significant changes in sGC abundance, cGMP-phosphodiesterase activity, or the vasorelaxant activity of protein kinase G.
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