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Chronic sodium nitrite therapy augments ischemia-induced angiogenesis and arteriogenesis
Open accessAbstract
Chronic tissue ischemia due to defective vascular perfusion is a hallmark feature of peripheral artery disease for which minimal therapeutic options exist. We have reported that sodium nitrite therapy exerts cytoprotective effects against acute ischemia/reperfusion injury in both heart and liver, consistent with the model of bioactive NO formation from nitrite during ischemic stress. Here, we test the hypothesis that chronic sodium nitrite therapy can selectively augment angiogenic activity and tissue perfusion in the murine hind-limb ischemia model. Various therapeutic doses (8.25-3,300 mug/kg) of sodium nitrite or PBS were administered. Sodium nitrite significantly restored ischemic hind-limb blood flow in a time-dependent manner, with low-dose sodium nitrite being most effective. Nitrite therapy significantly increased ischemic limb vascular density and stimulated endothelial cell proliferation. Remarkably, the effects of sodium nitrite therapy were evident within 3 days of the ischemic insult demonstrating the potency and efficacy of chronic sodium nitrite therapy. Sodium nitrite therapy also increased ischemic tissue nitrite and NO metabolites compared to nonischemic limbs. Use of the NO scavenger carboxy PTIO completely abolished sodium nitrite-dependent ischemic tissue blood flow and angiogenic activity consistent with nitrite reduction to NO being the proangiogenic mechanism. These data demonstrate that chronic sodium nitrite therapy is a recently discovered therapeutic treatment for peripheral artery disease and critical limb ischemia.
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In the citing paper
“In these experiments, nitrite conversion to nitric oxide was dependent on XOR.”
From Nitrate-Nitrite-Nitric Oxide Pathway: Implications for Anesthesiology and Intensive Care (2010) · cites this paper as [145]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Recently, inhaled nitrite has been shown to have beneficial effects in animal models of pulmonary hypertension.”
From Nitrate-Nitrite-Nitric Oxide Pathway: Implications for Anesthesiology and Intensive Care (2010) · cites this paper as [145]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Again, pulmonary hypertension was prevented by inhaled nitrite but also right ventricular hypertrophy and failure.”
From Nitrate-Nitrite-Nitric Oxide Pathway: Implications for Anesthesiology and Intensive Care (2010) · cites this paper as [145]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“In addition, hypoxia-induced proliferation of cultured pulmonary artery smooth muscle cells was inhibited by nitrite.”
From Nitrate-Nitrite-Nitric Oxide Pathway: Implications for Anesthesiology and Intensive Care (2010) · cites this paper as [145]
Experimental — accuracy not yet measuredIn the citing paper
“Nitrite is a dietary constituent that protects the heart against I/R injury in many animal models during both ischemia and preconditioning stage [186,187,188,189,190,191,192].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [191]
In the citing paper
“while nitrate supplementation prevents or limits ischemia-reperfusion injury and endothelial dysfunction in both animal[98,120–124] and human[97,125] models of ischemia-reperfusion.”
From Enterosalivary nitrate metabolism and the microbiome: Intersection of microbial metabolism, nitric oxide and diet in cardiac and pulmonary vascular health (2017) · cites this paper as [123]
In the citing paper
“This result is consistent with recent findings in studies investigating the role of nitrite injections in ischemia, 16 indicating that other nitrite-signaling pathways for regulating angiogenic activity may exist.20”
From Dietary nitrate supplementation improves revascularization in chronic ischemia (2012) · cites this paper as [16]
In the citing paper
“In ischemic angiogenesis, a continuous pharmacological intervention with nitrite injections resulted in an increased vascular density in the hind limb and stimulated endothelial cell proliferation.16”
From Dietary nitrate supplementation improves revascularization in chronic ischemia (2012) · cites this paper as [16]
In the citing paper
“Evidence for a role for NO is dependent largely on attenuation of responses by the NO-scavenger CPTIO [25, 26, 52, 100] and measurement of nitrite-dependent increases in cGMP levels[26, 101].”
From Current perspectives and challenges in understanding the role of nitrite as an integral player in nitric oxide biology and therapy (2011) · cites this paper as [100]
In the citing paper
“In some cases, increased nitrite levels are measured after administration, but in others no change in nitrite is observed despite clear evidence of NO-dependent signaling induction (a notable example being nitrite dependent stimulation of ischemic angiogenesis) [100, 123].”
From Current perspectives and challenges in understanding the role of nitrite as an integral player in nitric oxide biology and therapy (2011) · cites this paper as [100]
In the citing paper
“Conversely, nitrite is more concentrated within cells and tissues (low μM) compared to plasma [20, 46, 47].”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [47]
In the citing paper
“The potent effect of low doses of nitrite on limiting ischemia-reperfusion infarction suggests that nitrite may modulate critical pathophysiological stress responses, particularly those involved during tissue ischemia [47, 161].”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [47]
In the citing paper
“cPTIO treatment was shown by numerous groups to attenuate nitrite mediated protection against ischemia-reperfusion injury in vivo indicating that protective mechanisms likely involve NO dependent signaling pathways and molecular responses [47, 89, 156, 162].”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [47]
In the citing paper
“nitrite therapy selectively induced endothelial cell proliferation and angiogenesis only in the ischemic limb”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [47]
In the citing paper
“nitrite therapy significantly increased ischemic tissue nitrite/nitrosothiol levels”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [47]
In the citing paper
“sodium nitrate therapy was unable to mediate similar responses to nitrite therapy over the duration of study”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [47]
In the citing paper
“Our group has reported that continuous sodium nitrite administration increases ischemic hind limb blood flow after permanent femoral artery ligation.”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [47]
In the citing paper
“low dose sodium nitrite therapy quickly restored ischemic hind-limb blood flow within several days and did not affect flow in the contralateral non-ischemic limb”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [47]
In the citing paper
“nitrite mediated changes in blood flow and endothelial cell growth were blocked by the NO scavenger cPTIO”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [47]
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1 retracted
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Metadata
- Authors
- Kumar, D., Branch, B. G., Pattillo, C. B., Hood, J., Thoma, S., Simpson, S., Illum, S., Arora, N., Chidlow, J. H., Langston, W., Teng, X., Lefer, D. J., Patel, R. P., & Kevil, C. G.
- Affiliations
- Louisiana State University Health Sciences Center Shreveport (US)
- Departments of †Pathology and
- University of Alabama at Birmingham (US)
- Albert Einstein College of Medicine (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2008-05-27
- Volume
- 105
- Issue
- 21
- Pages
- 7540-7545
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2396555
- OpenAlex
- W2014848058
- Cited by
- 187
- References
- 49
- Citations by year
- 2025: 1 · 2024: 3 · 2023: 2 · 2022: 4 · 2021: 6 · 2020: 5 · 2019: 7 · 2018: 9 · 2017: 12 · 2016: 6 · 2015: 18 · 2014: 9 · 2013: 21 · 2012: 26
- FWCI
- 12.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL-80482, HL60849, R01HL080482, R01HL060849)
- National Institute of Diabetes and Digestive and Kidney Diseases (P01DK043785, DK-43785)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Surgery › Peripheral Artery Disease Management
- Keywords
- nitric oxide, angiogenesis, arteriogenesis, hindlimb ischemia, peripheral arterial disease, critical limb ischemia, ischemia-reperfusion injury, endothelial cell proliferation, vessel density, blood flow recovery
- MeSH terms
- Animals, Arteries, Cyclic N-Oxides, Disease Models, Animal, Endothelium, Vascular, Hindlimb, Imidazoles, Ischemia, Male, Mice, Inbred C57BL, Nitric Oxide, Sodium Nitrite, Free Radical Scavengers, Peripheral Vascular Diseases, Neovascularization, Physiologic, Cytoprotection, Mice
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