Nitric oxide bioavailability for red blood cell deformability in the microcirculation: A review of recent progress
The rheological properties of red blood cells (RBCs) play an important role in their microcirculation. RBCs can elastically deform in response to mechanical forces to pass through narrow vessels for effective gas exchange in peripheral tissues. Decreased RBC deformability is observed in lifestyle-re...
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Published in | Nitric Oxide Vol. 129; pp. 25 - 29 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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Elsevier Inc
01.12.2022
Elsevier BV |
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ISSN | 1089-8603 1089-8611 1089-8611 |
DOI | 10.1016/j.niox.2022.09.004 |
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Abstract | The rheological properties of red blood cells (RBCs) play an important role in their microcirculation. RBCs can elastically deform in response to mechanical forces to pass through narrow vessels for effective gas exchange in peripheral tissues. Decreased RBC deformability is observed in lifestyle-related diseases such as diabetes mellitus, hypercholesterolemia, and hypertension, which are pathological conditions linked to increased oxidative stress and decreased nitric oxide (NO) bioavailability. Redox-sensitive cysteine residues on RBC cytoskeletal proteins, such as α- and β-spectrins, responsible for membrane flexibility, are affected by prolonged oxidative stress, leading to reversible and irreversible oxidative modifications and decreased RBC deformability. However, endogenously, and exogenously generated NO protects RBC membrane flexibility from further oxidative modification by shielding redox-sensitive cysteine residues with a glutathione cap. Recent studies have shown that nitrate-rich diets and moderate exercise can enhance NO production to increase RBC deformability by increasing the interplay between RBCs and vascular endothelium-mediated NO bioavailability for microcirculation. This review focuses on the molecular mechanism of RBC- and non-RBC-mediated NO generation, and how diet- and exercise-derived NO exert prophylactic effects against decreased RBC deformability in lifestyle-related diseases with vascular endothelial dysfunction.
•The rheological properties of red blood cells (RBCs) play an important role in their microcirculation.•Decreased red blood cell deformability is observed in lifestyle-related diseases with increased oxidative stress and decreased nitric oxide (NO) bioavailability.•Endogenously and exogenously generated NO protect RBC membrane flexibility from oxidative modification.•RBC deformability is associated with the interplay between RBCs and vascular endothelium-mediated NO bioavailability. |
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AbstractList | The rheological properties of red blood cells (RBCs) play an important role in their microcirculation. RBCs can elastically deform in response to mechanical forces to pass through narrow vessels for effective gas exchange in peripheral tissues. Decreased RBC deformability is observed in lifestyle-related diseases such as diabetes mellitus, hypercholesterolemia, and hypertension, which are pathological conditions linked to increased oxidative stress and decreased nitric oxide (NO) bioavailability. Redox-sensitive cysteine residues on RBC cytoskeletal proteins, such as α- and β-spectrins, responsible for membrane flexibility, are affected by prolonged oxidative stress, leading to reversible and irreversible oxidative modifications and decreased RBC deformability. However, endogenously, and exogenously generated NO protects RBC membrane flexibility from further oxidative modification by shielding redox-sensitive cysteine residues with a glutathione cap. Recent studies have shown that nitrate-rich diets and moderate exercise can enhance NO production to increase RBC deformability by increasing the interplay between RBCs and vascular endothelium-mediated NO bioavailability for microcirculation. This review focuses on the molecular mechanism of RBC- and non-RBC-mediated NO generation, and how diet- and exercise-derived NO exert prophylactic effects against decreased RBC deformability in lifestyle-related diseases with vascular endothelial dysfunction.The rheological properties of red blood cells (RBCs) play an important role in their microcirculation. RBCs can elastically deform in response to mechanical forces to pass through narrow vessels for effective gas exchange in peripheral tissues. Decreased RBC deformability is observed in lifestyle-related diseases such as diabetes mellitus, hypercholesterolemia, and hypertension, which are pathological conditions linked to increased oxidative stress and decreased nitric oxide (NO) bioavailability. Redox-sensitive cysteine residues on RBC cytoskeletal proteins, such as α- and β-spectrins, responsible for membrane flexibility, are affected by prolonged oxidative stress, leading to reversible and irreversible oxidative modifications and decreased RBC deformability. However, endogenously, and exogenously generated NO protects RBC membrane flexibility from further oxidative modification by shielding redox-sensitive cysteine residues with a glutathione cap. Recent studies have shown that nitrate-rich diets and moderate exercise can enhance NO production to increase RBC deformability by increasing the interplay between RBCs and vascular endothelium-mediated NO bioavailability for microcirculation. This review focuses on the molecular mechanism of RBC- and non-RBC-mediated NO generation, and how diet- and exercise-derived NO exert prophylactic effects against decreased RBC deformability in lifestyle-related diseases with vascular endothelial dysfunction. The rheological properties of red blood cells (RBCs) play an important role in their microcirculation. RBCs can elastically deform in response to mechanical forces to pass through narrow vessels for effective gas exchange in peripheral tissues. Decreased RBC deformability is observed in lifestyle-related diseases such as diabetes mellitus, hypercholesterolemia, and hypertension, which are pathological conditions linked to increased oxidative stress and decreased nitric oxide (NO) bioavailability. Redox-sensitive cysteine residues on RBC cytoskeletal proteins, such as α- and β-spectrins, responsible for membrane flexibility, are affected by prolonged oxidative stress, leading to reversible and irreversible oxidative modifications and decreased RBC deformability. However, endogenously, and exogenously generated NO protects RBC membrane flexibility from further oxidative modification by shielding redox-sensitive cysteine residues with a glutathione cap. Recent studies have shown that nitrate-rich diets and moderate exercise can enhance NO production to increase RBC deformability by increasing the interplay between RBCs and vascular endothelium-mediated NO bioavailability for microcirculation. This review focuses on the molecular mechanism of RBC- and non-RBC-mediated NO generation, and how diet- and exercise-derived NO exert prophylactic effects against decreased RBC deformability in lifestyle-related diseases with vascular endothelial dysfunction. •The rheological properties of red blood cells (RBCs) play an important role in their microcirculation.•Decreased red blood cell deformability is observed in lifestyle-related diseases with increased oxidative stress and decreased nitric oxide (NO) bioavailability.•Endogenously and exogenously generated NO protect RBC membrane flexibility from oxidative modification.•RBC deformability is associated with the interplay between RBCs and vascular endothelium-mediated NO bioavailability. |
Author | Kobayashi, Jun Sonoda, Kunihiro Ohtake, Kazuo Murata, Isamu |
Author_xml | – sequence: 1 givenname: Jun orcidid: 0000-0002-3490-2980 surname: Kobayashi fullname: Kobayashi, Jun email: junkoba@josai.ac.jp organization: Department of Clinical Dietetics and Human Nutrition, Faculty of Pharmacy and Pharmaceutical Science, Josai University, Saitama, Japan – sequence: 2 givenname: Kazuo surname: Ohtake fullname: Ohtake, Kazuo email: kazuo@josai.ac.jp organization: Division of Physiology, School of Pharmaceutical Sciences, Faculty of Pharmacy and Pharmaceutical Science, Josai University, Saitama, Japan – sequence: 3 givenname: Isamu surname: Murata fullname: Murata, Isamu email: ismurata@josai.ac.jp organization: Laboratory of Pharmacotherapeutics and Neuropsychopharmacology, Faculty of Pharmaceutical Science, Josai University, Saitama, Japan – sequence: 4 givenname: Kunihiro surname: Sonoda fullname: Sonoda, Kunihiro email: naka-k@kinjo-u.ac.jp organization: Department of Food and Nutritional Environment, College of Human Life and Environment, Kinjo Gakuin University, Nagoya, Japan |
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Keywords | Oxidative stress Microcirculation Red blood cell deformability Exercise Diet Nitric oxide Redox Nitrite |
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