scholarly journals Roles of nitric oxide and shear stress in the regulation of microvessel permeability in intact rat mesenteric venules

2014 ◽  
Author(s):  
Sulei Xu
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Microvessel Permeability

Regulation of nitric oxide andbcl-2 expression by shear stress in human osteoarthritic chondrocytes in vitro

2003 ◽  
Vol 90 (1) ◽  
pp. 80-86 ◽  
Author(s):  
Mel S. Lee ◽  
Michael C.D. Trindade ◽  
Takashi Ikenoue ◽  
Stuart B. Goodman ◽  
David J. Schurman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Osteoarthritic Chondrocytes

Substance P increases microvascular permeability via nitric oxide-mediated convective pathways

1995 ◽  
Vol 268 (4) ◽  
pp. R1060-R1068 ◽  
Author(s):  
L. S. Nguyen ◽  
A. C. Villablanca ◽  
J. C. Rutledge
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Substance P ◽  
Microvascular Permeability ◽  
Nitric Oxide Production ◽  
Apparent Permeability ◽  
Substance P Receptor ◽  
Microvessel Permeability ◽  
Oxide Synthase ◽  
Quantitative Fluorescence

The goal of these studies was to examine the effects of substance P, a tachykinin neuropeptide, on pathways of microvascular permeability. Individual frog mesenteric venular capillaries were cannulated, and albumin apparent permeability coefficients (Ps) were determined by quantitative fluorescence microscopy. Ps of albumin (PsAlb) rose from 6.8 +/- 1.8 (SE) cm.s-1.10(7) at control to 22.3 +/- 2.3 cm.s-1.10(7) when substance P (10(-11) M) was perfused. The effect of increased microvessel permeability induced by substance P (10(-11) M) was blocked with the nonpeptide substance P receptor antagonist CP-96,345 and NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase. PsAlb increased 0.99 cm.s-1.10(7) for every cmH2O increase in microvessel pressure after treatment of the vessel with substance P, demonstrating coupling of albumin flux to transvascular water flow. In conclusion, the mechanism of increased microvessel permeability in response to substance P appears to be the result of receptor-mediated increase in nitric oxide production and formation of water-filled convective pathways presumably located between adjacent endothelial cells.

scholarly journals Nitric Oxide–Dependent and Nitric Oxide–Independent Transcriptional Responses to High Shear Stress in Endothelial Cells

Hypertension ◽  
2005 ◽  
Vol 45 (4) ◽  
pp. 672-680 ◽  
Author(s):  
Branko Braam ◽  
Remmert de Roos ◽  
Hans Bluyssen ◽  
Patrick Kemmeren ◽  
Frank Holstege ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Shear Stress ◽  
High Shear ◽  
High Shear Stress ◽  
Transcriptional Responses

Laminar Flow on Endothelial Cells Suppresses eNOS O-GlcNAcylation to Promote eNOS Activity

2021 ◽  
Author(s):  
Sarah Basehore ◽  
Samantha Bohlman ◽  
Callie Weber ◽  
Swathi Swaminathan ◽  
Yuji Zhang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Laminar Flow ◽  
No Production ◽  
Disturbed Flow ◽  
Enos Activity ◽  
Enos Phosphorylation ◽  
Steady Laminar ◽  
In Cells

Rationale: In diabetic animals as well as high glucose cell culture conditions, endothelial nitric oxide synthase (eNOS) is heavily O-GlcNAcylated, which inhibits its phosphorylation and nitric oxide (NO) production. It is unknown, however, whether varied blood flow conditions, which affect eNOS phosphorylation, modulate eNOS activity via O-GlcNAcylation-dependent mechanisms. Objective: The goal of this study was to test if steady laminar flow, but not oscillating disturbed flow, decreases eNOS O-GlcNAcylation, thereby elevating eNOS phosphorylation and NO production. Methods and Results: Human umbilical vein endothelial cells (HUVEC) were exposed to either laminar flow (20 dynes/cm2 shear stress) or oscillating disturbed flow (4{plus minus}6 dynes/cm2 shear stress) for 24 hours in a cone-and-plate device. eNOS O-GlcNAcylation was almost completely abolished in cells exposed to steady laminar but not oscillating disturbed flow. Interestingly, there was no change in protein level or activity of key O-GlcNAcylation enzymes (OGT, OGA, or GFAT). Instead, metabolomics data suggest that steady laminar flow decreases glycolysis and hexosamine biosynthetic pathway (HBP) activity, thereby reducing UDP-GlcNAc pool size and consequent O-GlcNAcylation. Inhibition of glycolysis via 2-deoxy-2-glucose (2-DG) in cells exposed to disturbed flow efficiently decreased eNOS O-GlcNAcylation, thereby increasing eNOS phosphorylation and NO production. Finally, we detected significantly higher O-GlcNAcylated proteins in endothelium of the inner aortic arch in mice, suggesting that disturbed flow increases protein O-GlcNAcylation in vivo. Conclusions: Our data demonstrate that steady laminar but not oscillating disturbed flow decreases eNOS O-GlcNAcylation by limiting glycolysis and UDP-GlcNAc substrate availability, thus enhancing eNOS phosphorylation and NO production. This research shows for the first time that O-GlcNAcylation is regulated by mechanical stimuli, relates flow-induced glycolytic reductions to macrovascular disease, and highlights targeting HBP metabolic enzymes in endothelial cells as a novel therapeutic strategy to restore eNOS activity and prevent EC dysfunction in cardiovascular disease.

Nitric oxide limits coronary vasoconstriction by a shear stress-dependent mechanism

2001 ◽  
Vol 281 (2) ◽  
pp. H796-H803 ◽  
Author(s):  
David W. Stepp ◽  
Daphne Merkus ◽  
Yasuhiro Nishikawa ◽  
William M. Chilian
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Coronary Microcirculation ◽  
Shear Stresses ◽  
No Production ◽  
Small Arteries ◽  
Inner Diameter ◽  
Stress Dependent ◽  
Dependent Mechanism

Increases in shear stress promote coronary vasodilation by stimulating the production of nitric oxide (NO). Whether shear stress-induced NO production also limits vasoconstriction in the coronary microcirculation in vivo is unknown. Accordingly, we measured microvascular diameter and flow velocity in the beating heart along with estimated blood viscosity to calculate shear stress during vasoconstriction with endothelin or vasopressin. Measurements were repeated in the presence of N G-monomethyl-l-arginine (l-NMMA) to inhibit NO production and BQ-788 to block NO-linked endothelin type B receptors. BQ-788 did not augment steady-state constriction to endothelin, suggesting that NO production via activation of this receptor is inconsequential. l-NMMA potentiated constriction to both agonists, particularly in small arteries (inner diameter >120 μm). Shear stresses in small arteries were elevated during constriction and further elevated during constriction after l-NMMA. These observations suggest that NO production limits vasoconstriction in the coronary microcirculation and that the principal stimulus for this governance is elevated shear stress. The degree of shear stress moderation of constriction is heterogeneously distributed, with small arteries displaying a higher degree of shear stress regulation than arterioles. These results provide the strongest evidence to date that shear stress-mediated production of NO exerts a “braking” influence on constriction in the coronary microcirculation.

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
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