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 inNitric Oxide Vol. 129; pp. 25 - 29
Main Authors Kobayashi, Jun, Ohtake, Kazuo, Murata, Isamu, Sonoda, Kunihiro
Format Journal Article
LanguageEnglish
Published Elsevier Inc 01.12.2022
Elsevier BV
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ISSN1089-8603
1089-8611
1089-8611
DOI10.1016/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.
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
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Keywords Oxidative stress
Microcirculation
Red blood cell deformability
Exercise
Diet
Nitric oxide
Redox
Nitrite
Language English
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Snippet The rheological properties of red blood cells (RBCs) play an important role in their microcirculation. RBCs can elastically deform in response to mechanical...
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SubjectTerms Cysteine
Diet
Erythrocyte Deformability
Erythrocytes
Exercise
Microcirculation
Nitric Oxide
Nitrite
Oxidative stress
Red blood cell deformability
Redox
Title Nitric oxide bioavailability for red blood cell deformability in the microcirculation: A review of recent progress
URI https://dx.doi.org/10.1016/j.niox.2022.09.004
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