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Cited by 72Nitric Oxide and Endothelin EffectsHemoglobin structure and functionIron Metabolism and Disorders

Up-regulation of renal and vascular nitric oxide synthase in iron-deficiency anemia

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Ni, Zhenmin, Morcos, Samer, Vaziri, Nosratola D.·1997·Kidney International
DOI 10.1038/ki.1997.319
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Abstract

Anemia is frequently associated with increased cardiac output and reduced vascular resistance. The latter has been attributed to reduced inactivation of nitric oxide (NO) by hemoglobin. We hypothesized that in addition to reducing NO inactivation, anemia may up-regulate NO production. To test this hypothesis, male Sprague-Dawley rats with chronic iron-deficiency anemia (produced by multiple phlebotomies and an iron-free diet) were studied. The results were compared with those obtained in a group of normal control animals. The anemic group showed marked increases in urinary excretion, plasma concentration, and renal and aorta tissue contents of NO metabolites (total nitrates and nitrites, NOx). This was accompanied by a significant rise in urinary excretion of cGMP, the second messenger for NO. In addition, NO synthase (NOS) activity and endothelial constitutive (ecNOS) and inducible NOS (iNOS) proteins of the thoracic aorta were markedly increased in the anemic group. Likewise, renal tissue ecNOS and iNOS proteins were greatly increased in the anemic animals. NOS activity and protein values were inversely related to hematocrit and directly related to plasma, tissue and urinary NOx. The constellation of these findings points to an increased NOS expression and NO production as opposed to the mere reduction of NO inactivation in iron-deficiency anemia. Further studies are planned to determine the mechanism of NOS up-regulation in iron-deficiency anemia.

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Crossref · 10.1038/ki.1997.319

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  • Decreased hematocrit due to iron deficiency anemia may decrease RBC-mediated NO scavenging, leading to hypotension.

    “On the other hand, it was shown that a decreased hematocrit due to iron deficiency anemia may decrease RBC-mediated NO scavenging, leading to hypotension (140).”

    From Red Blood Cell Function and Dysfunction: Redox Regulation, Nitric Oxide Metabolism, Anemia (2017) · cites this paper as [140]

  • In a rat model of iron deficiency anemia, expression and activity of eNOS were increased in the aorta and in the kidney.

    “In a rat model of iron deficiency anemia, expression and activity of eNOS were increased in the aorta and in the kidney (140), pointing to a further mechanism leading to increase in NO bioavailability in anemia.”

    From Red Blood Cell Function and Dysfunction: Redox Regulation, Nitric Oxide Metabolism, Anemia (2017) · cites this paper as [140]

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Authors
Ni, Z., Morcos, S., & Vaziri, N. D.
Affiliations
University of California, Irvine (US)
ORCID
Vaziri, Nosratola D.
Venue
Kidney International
Publisher
Elsevier BV
Published
1997-07
Volume
52
Issue
1
Pages
195-201
ISSN
0085-2538 (ISSN-L)
DOI
10.1038/ki.1997.319
OpenAlex
W1988140295
Cited by
72
References
16
Citations by year
2025: 1 · 2024: 2 · 2023: 2 · 2020: 3 · 2019: 3 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 1 · 2014: 1 · 2013: 4
FWCI
3.05
Type
journal article
Language
en
Open access
Licence
Locations
  • Kidney International (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hemoglobin structure and function
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
Keywords
iron deficiency anemia, nitric oxide synthase, nitric oxide, inducible nitric oxide synthase, constitutive nitric oxide synthase, renal nitric oxide, cyclic GMP, hemoglobin, hematocrit, vascular resistance, cardiac output
MeSH terms
Animals, Cyclic GMP, Kidney, Male, Nitrates, Nitric Oxide, Nitrites, Blotting, Western, Up-Regulation, Rats, Sprague-Dawley, Anemia, Iron-Deficiency, Nitric Oxide Synthase, Rats

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