ArticleJournal of theoretical biology2013
Contribution of membrane permeability and unstirred layer diffusion to nitric oxide-red blood cell interaction.
Article in Journal of theoretical biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Role of channels in thebioRxiv : the preprint server for biology · 2025Article
- Nitric oxide modelling and its bioavailability influenced by red blood cells.Journal of the Royal Society, Interface · 2024Article
- Cardiovascular "Patterns" of HBiomolecules · 2021Article
- Modulation of Local and Systemic Heterocellular Communication by Mechanical Forces: A Role of Endothelial Nitric Oxide Synthase.Antioxidants & redox signaling · 2017Review
- Red Blood Cell Function and Dysfunction: Redox Regulation, Nitric Oxide Metabolism, Anemia.Antioxidants & redox signaling · 2017Review
- Accelerated RBC senescence as a novel pathologic mechanism of blood stasis syndrome in traditional East Asian medicine.American journal of translational research · 2015Review
- Endothelial NO and O₂·⁻ production rates differentially regulate oxidative, nitroxidative, and nitrosative stress in the microcirculation.Free radical biology & medicine · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Nitric oxide (NO) consumption by red blood cell (RBC) hemoglobin (Hb) in vasculature is critical in regulating the vascular tone. The paradox of NO production at endothelium in close proximity of an effective NO scavenger Hb in RBCs is mitigated by lower NO consumption by RBCs compared to that of free Hb due to transport resistances including membrane resistance, extra- and intra-cellular resistances for NO biotransport to the RBC. Relative contribution of each transport resistance on NO-RBC interactions is still not clear. We developed a mathematical model of NO transport to a single RBC to quantify the contributions from individual transport barriers by analyzing the effect of RBC membrane permeability (P(m)), hematocrit (Hct) and NO-Hb reaction rate constants on NO-RBC interactions. Our results indicated that intracellular diffusion of NO was not a rate limiting step for NO-RBC interactions. The extracellular diffusion contributed 70-90% of total transport resistance for P(m)>1 cm s(-1) whereas membrane resistance accounts for 50-75% of total transport resistance for P(m)<0.1 cm s(-1). We propose a narrow P(m) range of 0.21-0.44 cm s(-1) for 10-45% Hct, respectively, below which membrane resistance is more significant and above which extracellular diffusion is a dominating transport resistance for NO-RBC interactions.
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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.