Tags

Type your tag names separated by a space and hit enter

Regulation of red blood cell deformability is independent of red blood cell-nitric oxide synthase under hypoxia.
Clin Hemorheol Microcirc. 2016 Sep 12; 63(3):199-215.CH

Abstract

The aim was to study impacts of mild to severe hypoxia on human red blood cell (RBC)-nitric oxide synthase (NOS)-dependent NO production, protein S-nitrosylation and deformability.Ambient air oxygen concentration of 12 healthy subjects was step-wisely reduced from 20.95% to 16.21%, 12.35%, 10% and back to 20.95%. Additional in vitro experiments involved purging of blood (±sodium nitrite) with gas mixtures corresponding to in vivo intervention.Vital and hypoxia-associated parameters showed physiological adaptation to changing demands. Activation of RBC-NOS decreased with increasing hypoxia. RBC deformability, which is influenced by RBC-NOS activation, decreased under mild hypoxia, but surprisingly increased at severe hypoxia in vivo and in vitro. This was causatively induced by nitrite reduction to NO which increased S-nitrosylation of RBC α- and β-spectrins -a critical step to improve RBC deformability. The addition of sodium nitrite prevented decreases of RBC deformability under hypoxia by sustaining S-nitrosylation of spectrins suggesting compensatory mechanisms of non-RBC-NOS-produced NO.The results first time indicate a direct link between maintenance of RBC deformability under severe hypoxia by non-enzymatic NO production because RBC-NOS activation is reduced. These data improve our understanding of physiological mechanisms supporting adequate blood and, thus, oxygen supply to different tissues under severe hypoxia.

Authors+Show Affiliations

Department of Molecular and Cellular Sport Medicine, German Sport University Cologne, Germany. The German Research Center of Elite Sport (momentum), German Sport University Cologne, Germany.Department of Internal Medicine I (Cardiology, Angiology, Pneumology), Friedrich-Schiller University, Jena, Germany.Department of Molecular and Cellular Sport Medicine, German Sport University Cologne, Germany.Department of Internal Medicine I (Cardiology, Angiology, Pneumology), Friedrich-Schiller University, Jena, Germany.Department of Molecular and Cellular Sport Medicine, German Sport University Cologne, Germany.Department of Internal Medicine I (Cardiology, Angiology, Pneumology), Friedrich-Schiller University, Jena, Germany.Department of Molecular and Cellular Sport Medicine, German Sport University Cologne, Germany. The German Research Center of Elite Sport (momentum), German Sport University Cologne, Germany.Department of Molecular and Cellular Sport Medicine, German Sport University Cologne, Germany. The German Research Center of Elite Sport (momentum), German Sport University Cologne, Germany.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

26890238

Citation

Grau, Marijke, et al. "Regulation of Red Blood Cell Deformability Is Independent of Red Blood Cell-nitric Oxide Synthase Under Hypoxia." Clinical Hemorheology and Microcirculation, vol. 63, no. 3, 2016, pp. 199-215.
Grau M, Lauten A, Hoeppener S, et al. Regulation of red blood cell deformability is independent of red blood cell-nitric oxide synthase under hypoxia. Clin Hemorheol Microcirc. 2016;63(3):199-215.
Grau, M., Lauten, A., Hoeppener, S., Goebel, B., Brenig, J., Jung, C., Bloch, W., & Suhr, F. (2016). Regulation of red blood cell deformability is independent of red blood cell-nitric oxide synthase under hypoxia. Clinical Hemorheology and Microcirculation, 63(3), 199-215. https://doi.org/10.3233/CH-162044
Grau M, et al. Regulation of Red Blood Cell Deformability Is Independent of Red Blood Cell-nitric Oxide Synthase Under Hypoxia. Clin Hemorheol Microcirc. 2016 Sep 12;63(3):199-215. PubMed PMID: 26890238.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of red blood cell deformability is independent of red blood cell-nitric oxide synthase under hypoxia. AU - Grau,Marijke, AU - Lauten,Alexander, AU - Hoeppener,Steffen, AU - Goebel,Bjoern, AU - Brenig,Julian, AU - Jung,Christian, AU - Bloch,Wilhelm, AU - Suhr,Frank, PY - 2016/2/19/entrez PY - 2016/2/19/pubmed PY - 2017/2/17/medline KW - Humans KW - nitric oxide KW - normobaric hypoxia KW - red blood cell deformability KW - red blood cell-nitric oxide synthase KW - red blood cells SP - 199 EP - 215 JF - Clinical hemorheology and microcirculation JO - Clin Hemorheol Microcirc VL - 63 IS - 3 N2 - The aim was to study impacts of mild to severe hypoxia on human red blood cell (RBC)-nitric oxide synthase (NOS)-dependent NO production, protein S-nitrosylation and deformability.Ambient air oxygen concentration of 12 healthy subjects was step-wisely reduced from 20.95% to 16.21%, 12.35%, 10% and back to 20.95%. Additional in vitro experiments involved purging of blood (±sodium nitrite) with gas mixtures corresponding to in vivo intervention.Vital and hypoxia-associated parameters showed physiological adaptation to changing demands. Activation of RBC-NOS decreased with increasing hypoxia. RBC deformability, which is influenced by RBC-NOS activation, decreased under mild hypoxia, but surprisingly increased at severe hypoxia in vivo and in vitro. This was causatively induced by nitrite reduction to NO which increased S-nitrosylation of RBC α- and β-spectrins -a critical step to improve RBC deformability. The addition of sodium nitrite prevented decreases of RBC deformability under hypoxia by sustaining S-nitrosylation of spectrins suggesting compensatory mechanisms of non-RBC-NOS-produced NO.The results first time indicate a direct link between maintenance of RBC deformability under severe hypoxia by non-enzymatic NO production because RBC-NOS activation is reduced. These data improve our understanding of physiological mechanisms supporting adequate blood and, thus, oxygen supply to different tissues under severe hypoxia. SN - 1875-8622 UR - https://www.unboundmedicine.com/medline/citation/26890238/Regulation_of_red_blood_cell_deformability_is_independent_of_red_blood_cell_nitric_oxide_synthase_under_hypoxia_ DB - PRIME DP - Unbound Medicine ER -