ArticleCirculation research2008
Hypoxic vasodilation by red blood cells: evidence for an s-nitrosothiol-based signal.
Article in Circulation research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 145 citations in OpenAlex.
- Main events and mechanism of human erythrocyte ageing.Expert reviews in molecular medicine · 2026Review
- NO- and S-nitrosothiols-dependent relaxation in large and small resistance blood vessels.Frontiers in physiology · 2026Review
- Piezo1 activates nitric oxide synthase in red blood cells via protein kinase C with increased activity in diabetes.Mechanobiology in medicine · 2025Article
- PGRMC2 is a pressure-volume regulator critical for myocardial responses to stress in mice.Nature communications · 2025Article
- Stimulation of Erythrocyte Soluble Guanylyl Cyclase Induces cGMP Export and Cardioprotection in Type 2 Diabetes.JACC. Basic to translational science · 2023Article
- Optimized S-nitrosohemoglobin Synthesis in Red Blood Cells to Preserve Hypoxic Vasodilation ViaThe Journal of pharmacology and experimental therapeutics · 2022Article
- On the Role of Dietary Nitrate in the Maintenance of Systemic and Oral Health.Dentistry journal · 2022Review
- Nitric Oxide Production and Regulation in the Teleost Cardiovascular System.Antioxidants (Basel, Switzerland) · 2022Review
- The role of globins in cardiovascular physiology.Physiological reviews · 2022Review
- The enzymatic function of the honorary enzyme: S-nitrosylation of hemoglobin in physiology and medicine.Molecular aspects of medicine · 2022Review
- Hypoxic vasodilatory defect and pulmonary hypertension in mice lacking hemoglobin β-cysteine93 S-nitrosylation.JCI insight · 2022Article
- Effects of Nitrate Supplementation on Exercise Performance in Humans: A Narrative Review.Nutrients · 2021Review
- Integrated pancreatic microcirculatory profiles of streptozotocin-induced and insulin-administrated type 1 diabetes mellitus.Microcirculation (New York, N.Y. : 1994) · 2021Article
- Genomic Insights into the Origin and Evolution of Molluscan Red-Bloodedness in the Blood Clam Tegillarca granosa.Molecular biology and evolution · 2021Article
- Hypoxic pulmonary vasoconstriction as a regulator of alveolar-capillary oxygen flux: A computational model of ventilation-perfusion matching.PLoS computational biology · 2021Article
- Red Blood Cell-Mediated S-Nitrosohemoglobin-Dependent Vasodilation: Lessons Learned from a β-Globin Cys93 Knock-In Mouse.Antioxidants & redox signaling · 2021Review
- Endurance of erythrocyte series in chemotherapy.Experimental and therapeutic medicine · 2020Article
- Multimodal Device and Computer Algorithm-Based Monitoring of Pancreatic Microcirculation Profiles In Vivo.Pancreas · 2020Article
- CRISPR-engineered human brown-like adipocytes prevent diet-induced obesity and ameliorate metabolic syndrome in mice.Science translational medicine · 2020Article
- Essential Role of Hemoglobin βCys93 in Cardiovascular Physiology.Physiology (Bethesda, Md.) · 2020Review
13 more citing papers are in PubMed but not listed here.
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3 authors at 1 institution in 1 country.
Funding
Abstract
Red blood cells (RBCs) have been ascribed an essential role in matching blood flow to local metabolic demand during hypoxic vasodilation. The vasodilatory function of RBCs evidently relies on the allosteric properties of hemoglobin (Hb), which couple the conformation of Hb to tissue oxygen tension (Po(2)) and thereby provide a basis for the graded vasodilatory activity that is inversely proportional to Hb oxygen saturation. Although a large body of evidence indicates that the Po(2)-coupled allosteric transition from R (oxy)-state to T (deoxy)-state subserves the release from Hb of vasodilatory nitric oxide (NO) bioactivity, it has not yet been determined whether the NO-based signal is a necessary and sufficient source of RBC-mediated vasoactivity and it has been suggested that ATP or nitrite may also contribute. We demonstrate here by bioassay that untreated human RBCs rapidly and substantially relax thoracic aorta from both rabbit and mouse at low Po(2) (approximately 1% O(2)) but not at high Po(2) (approximately 21% O(2)). RBC-mediated vasorelaxation is inhibited by prior depletion of S-nitroso-Hb, potentiated by low-molecular-weight thiols, and dependent on cGMP. Furthermore, these relaxations are largely endothelium-independent and unaffected by NO synthase inhibition or nitrite. Robust relaxations by RBCs are also elicited in the absence of endothelial, neuronal or inducible NO synthase. Finally, contractions that appear following resolution of RBC-mediated relaxations are dependent on NO derived from RBCs as well as the endothelium. Our results suggest that an S-nitrosothiol-based signal originating from RBCs mediates hypoxic vasodilation by RBCs, and that vasorelaxation by RBCs dominates NO-based vasoconstriction under hypoxic conditions.
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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.