Effects of nitric oxide on red blood cell deformability.
@article{BorKucukatay2003EffectsON,
title={Effects of nitric oxide on red blood cell deformability.},
author={Melek Bor-Kucukatay and Rosalinda B. Wenby and Herbert J. Meiselman and Oguz K. Baskurt},
journal={American journal of physiology. Heart and circulatory physiology},
year={2003},
volume={284 5},
pages={
H1577-84
}
}In addition to its known action on vascular smooth muscle, nitric oxide (NO) has been suggested to have cardiovascular effects via regulation of red blood cell (RBC) deformability. The present study was designed to further explore this possibility. Human RBCs in autologous plasma were incubated for 1 h with NO synthase (NOS) inhibitors [N(omega)-nitro-l-arginine methyl ester (l-NAME) and S-methylisothiourea], NO donors [sodium nitroprusside (SNP) and diethylenetriamine (DETA)-NONOate], an NO…
258 Citations
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It could be mentioned that endogenous or exogenous NO in the model applied in this study may not have a decisive impact on blood coagulation process, however, the non-specific effects observed in the L-Arginine + L-NAME group on the number of red blood cells and hemoglobin concentration need further studies.
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It is suggested that NO may prevent mechanical deterioration of RBC exposed to high shear stresses and might be mediated by the inhibition of potassium leakage from RBC.
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Evidence is provided that RBCs from humans express an active and functional endothelial-type NOS (eNOS), which is localized in the plasma membrane and the cytoplasm of R BCs, which is regulated by its substrate L-arginine, by calcium, and by phosphorylation via PI3 kinase.
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This study for the first time showed highest basal RBC-NOS activation in ESRD-RBCs, possibly to reduce the negative impact of decreased NOS expression, and it is further conceivable that high NO production only partially affects cell function of ESRDs because in vivo they are unable to respond to physiologic stimuli, such as calcium and/or insulin.
Nitric oxide influences red blood cell velocity independently of changes in the vascular tone
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Results indicate that scavenging of NO and inhibition of NO synthesis decrease RBC velocity not only by regulating vascular tone but also by decreasing RBC deformability.
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Since the identification of the elusive endothelium-derived relaxing factor as nitric oxide (NO), much attention has been devoted to understanding its physiological effects. NO is a free radical with…
RBC-NOS-Dependent S-Nitrosylation of Cytoskeletal Proteins Improves RBC Deformability
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This study first-time provides strong evidence that RBC-NOS-produced NO modifies RBC deformability through direct S-nitrosylation of cytoskeleton proteins, most likely α- and β-spectrins.
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