Regulation of red blood cell deformability is independent of red blood cell-nitric oxide synthase under hypoxia
| Autor: | Bjoern Goebel, Frank Suhr, Marijke Grau, Julian Brenig, Alexander Lauten, Steffen Hoeppener, Wilhelm Bloch, Christian Jung |
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| Přispěvatelé: | Jung, F, Jung, C |
| Rok vydání: | 2016 |
| Předmět: |
Adult
Male 0301 basic medicine medicine.medical_specialty Erythrocytes Endothelium Physiology 030204 cardiovascular system & hematology Nitric Oxide Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Erythrocyte Deformability Physiology (medical) Internal medicine medicine Humans Erythrocyte deformability Nitrite Sodium nitrite biology Hematology S-Nitrosylation Cell Hypoxia Nitric oxide synthase Red blood cell 030104 developmental biology Endocrinology medicine.anatomical_structure chemistry biology.protein Nitric Oxide Synthase Cardiology and Cardiovascular Medicine |
| Zdroj: | Clinical Hemorheology and Microcirculation. 63:199-215 |
| ISSN: | 1875-8622 1386-0291 |
| DOI: | 10.3233/ch-162044 |
| Popis: | 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. ispartof: Clinical Hemorheology and Microcirculation vol:63 issue:3 pages:199-215 ispartof: location:Netherlands status: published |
| Databáze: | OpenAIRE |
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