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Cited by 17Nitric Oxide and Endothelin EffectsPulmonary Hypertension Research and TreatmentsRedox biology and oxidative stress

Redox regulation of responses to hypoxia and NO–cGMP signaling in pulmonary vascular pathophysiology

Wolin, Michael S., Gupte, Sachin A., Mingone, Christopher J., Neo, Boon Hwa, Gao, Qun, Ahmad, Mansoor·2010·Annals of the New York Academy of Sciences
DOI 10.1111/j.1749-6632.2010.05557.x
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Abstract

Pulmonary vascular responses elicited by hypoxia and NO-cGMP signaling are potentially influenced by ROS and redox mechanisms that change during the progression of disease processes. Our studies in endothelium-rubbed bovine pulmonary arteries suggest increased glucose-6-phosphate dehydrogenase levels (compared to coronary arteries) seem to maintain a tonic peroxide-mediated relaxation removed by hypoxia through NADPH fueling superoxide generation from Nox oxidase. The activities of glucose-6-phosphate dehydrogenase, oxidases (i.e., Nox4), and systems metabolizing superoxide and peroxide markedly influence hypoxic pulmonary vasoconstriction (HPV). Activation of soluble guanylate cyclase and cGMP protein kinase seems to participate in peroxide-elicited relaxation. Endogenous NO helps maintain low pulmonary arterial pressure and suppresses HPV. Multiple redox processes potentially occurring during the progression of pulmonary hypertension may also attenuate NO-mediated relaxation beyond its scavenging by superoxide, including oxidation of guanylate cyclase heme and thiols normally maintained by cytosolic NADPH redox control.

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Crossref · 10.1111/j.1749-6632.2010.05557.x

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Authors
Wolin, M. S., Gupte, S. A., Mingone, C. J., Neo, B. H., Gao, Q., & Ahmad, M.
Affiliations
  • New York Medical College (US)
  • University of South Alabama (US)
Corresponding author
Wolin, Michael S.
ORCID
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2010-08
Volume
1203
Issue
1
Pages
126-132
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
DOI
10.1111/j.1749-6632.2010.05557.x
OpenAlex
W1589742730
Cited by
17
References
37
Citations by year
2020: 3 · 2018: 1 · 2017: 2 · 2016: 1 · 2015: 2 · 2014: 1 · 2013: 3 · 2012: 2
FWCI
0.23
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 16 d)
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (R01HL132574, P01HL043023, HL043023, R01HL066331, HL085352, R01HL085352, HL031069, R01HL031069, HL066331)
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords
redox regulation, hypoxia, nitric oxide, cGMP signaling, pulmonary hypertension, pulmonary vasoconstriction, reactive oxygen species, superoxide, NADPH, glucose-6-phosphate dehydrogenase, NOX4, soluble guanylate cyclase, thiols, pulmonary artery, endothelium
MeSH terms
Animals, Hypoxia, Cyclic GMP, Humans, Nitric Oxide, Oxidation-Reduction, Pulmonary Artery, Signal Transduction

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