Shear-stress mediated nitric oxide production within red blood cells: A dose-response

2019 ◽  
Vol 71 (2) ◽  
pp. 203-214 ◽  
Author(s):  
Jarod T. Horobin ◽  
Nobuo Watanabe ◽  
Masaya Hakozaki ◽  
Surendran Sabapathy ◽  
Michael J. Simmonds
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Red Blood Cells ◽  
Dose Response ◽  
Blood Cells ◽  
Nitric Oxide Production ◽  
Oxide Production

scholarly journals In Silico Modeling of Shear-Stress-Induced Nitric Oxide Production in Endothelial Cells through Systems Biology

2013 ◽  
Vol 104 (10) ◽  
pp. 2295-2306 ◽  
Author(s):  
Andrew Koo ◽  
David Nordsletten ◽  
Renato Umeton ◽  
Beracah Yankama ◽  
Shiva Ayyadurai ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Systems Biology ◽  
In Silico ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
In Silico Modeling

scholarly journals Shear stress activation of nitric oxide synthase and increased nitric oxide levels in human red blood cells

Nitric Oxide ◽  
2011 ◽  
Vol 24 (4) ◽  
pp. 184-191 ◽  
Author(s):  
Pinar Ulker ◽  
Nazmi Yaras ◽  
Ozlem Yalcin ◽  
Ciler Celik-Ozenci ◽  
Paul C. Johnson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Nitric Oxide Synthase ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Human Red Blood Cells ◽  
Oxide Synthase ◽  
Stress Activation

Dose Response Study of Laser Therapy on Nitric Oxide Production in Macrophages

2014 ◽  
Vol 117 (2) ◽  
pp. e196-e197
Author(s):  
SAMANTHA CARDOSO DE ANDRADE ◽  
IGOR HENRIQUE MORAIS SILVA ◽  
WYLLA TATIANA FERREIRA E SILVA ◽  
RAUL MANHÃES DE CASTRO ◽  
LUIZ ALCINO MONTEIRO GUEIROS ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Laser Therapy ◽  
Dose Response ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
Dose Response Study

scholarly journals PO-277 Nitric oxide generation in red blood cells induced by exercise

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Zhenghui Zha ◽  
Yuli Zhang
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Red Blood Cells ◽  
Blood Vessels ◽  
Blood Cells ◽  
White Blood Cells ◽  
Pi3k Pathway ◽  
No Production ◽  
Hemodynamic Changes ◽  
Enzyme Source

Objective Vascular endothelial nitric oxide synthase (NOS) is considered to be the main enzyme source for NO production in blood vessels, and studies have shown that RBC may also express NOS and produce NO. The purpose of this study was to summarize the expression of NOS in vascular red blood cells caused by changes in hemodynamics, and to improve the bioavailability of NO, and to lay a theoretical foundation for exploring the mechanism of exercise to improve vasodilation. Methods A literature review method was used to analyze related studies on exercise and RBC-NOS published in recent years. Results Intravascular NO is one of the most important vascular signaling molecules, which has the function of relaxing blood vessels. NO is produced during the conversion of L-arginine into L-citrulline, which is mainly dependent on the regulation of vascular eNOS. RBC can express NOS under certain action, and RBC-NOS is mainly located on RBC membrane and cytoplasm; The regulatory mechanisms of RBC-NOS and eNOS have similarities and differences: RBC-NOS and eNOS are both dependent on Ca2+ regulation and phosphorylation of Serine 1177  via the PI3K pathway; however, since red blood cells do not have nuclei, endoplasmic reticulum and Golgi, they do not have other mechanisms of action of eNOS. Therefore, the vascular endothelium is not the only source of NO production. Red blood cells, white blood cells and platelets can produce NO. The amount of NO produced by red blood cells is significantly higher than that of white blood cells and platelets，it is another major source of NO production in blood vessels.The level of wall shear stress is the main determinant of NOS expression in blood vessels: On the one hand, exercise training can cause hemodynamic changes, increased shear stress, and induce changes in eNOS and RBC-NOS levels, increase NO bioavailability, and participate in the regulation of vasodilation.On the other hand, moderate-intensity exercise causes NO produced by RBC to increase red blood cell deformability and participate in vascular regulation. Conclusions 1.Erythrocyte is an enzyme source that relies on hemodynamics to release NO from the blood vessel wall. It is regulated by Ca2+ and phosphorylates ser1177 through the PI3K pathway to participate in the regulation of the body. 2.Hemodynamic changes caused by exercise training can simultaneously induce the expression of eNOS and RBC-NOS, increase the bioavailability of NO, and jointly mediate vasodilation.

Gene Expression of Endothelial Cells under Pulsatile Non-Reversing vs. Steady Shear Stress; Comparison of Nitric Oxide Production

2008 ◽  
Vol 36 (4) ◽  
pp. 571-579 ◽  
Author(s):  
Andrew Yee ◽  
Kami A. Bosworth ◽  
Daniel E. Conway ◽  
Suzanne G. Eskin ◽  
Larry V. McIntire
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Steady Shear ◽  
Nitric Oxide Production ◽  
Oxide Production
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