scholarly journals Shear Stress-Triggered Nitric Oxide Release From Schlemm's Canal Cells

2014 ◽  
Vol 55 (12) ◽  
pp. 8067-8076 ◽  
Author(s):  
N. E. Ashpole ◽  
D. R. Overby ◽  
C. R. Ethier ◽  
W. D. Stamer
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Schlemm’S Canal ◽  
Nitric Oxide Release ◽  
Schlemm's Canal

scholarly journals Shear Stress in Schlemm’s Canal as a Sensor of Intraocular Pressure

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Fiona McDonnell ◽  
Kristin M. Perkumas ◽  
Nicole E. Ashpole ◽  
Joan Kalnitsky ◽  
Joseph M. Sherwood ◽  
...  
Keyword(s):  
Shear Stress ◽  
Intraocular Pressure ◽  
Schlemm’S Canal ◽  
Schlemm's Canal

scholarly journals Role of nitric oxide in murine conventional outflow physiology

2015 ◽  
Vol 309 (4) ◽  
pp. C205-C214 ◽  
Author(s):  
Jason Y. H. Chang ◽  
W. Daniel Stamer ◽  
Jacques Bertrand ◽  
A. Thomas Read ◽  
Catherine M. Marando ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Fluorescent Protein ◽  
Detectable Effect ◽  
No Production ◽  
Schlemm’S Canal ◽  
Physiological Regulation ◽  
Outflow Facility ◽  
Aqueous Humor Outflow ◽  
Schlemm's Canal

Elevated intraocular pressure (IOP) is the main risk factor for glaucoma. Exogenous nitric oxide (NO) decreases IOP by increasing outflow facility, but whether endogenous NO production contributes to the physiological regulation of outflow facility is unclear. Outflow facility was measured by pressure-controlled perfusion in ex vivo eyes from C57BL/6 wild-type (WT) or transgenic mice expressing human endothelial NO synthase (eNOS) fused to green fluorescent protein (GFP) superimposed on the endogenously expressed murine eNOS (eNOS-GFPtg). In WT mice, exogenous NO delivered by 100 μM S-nitroso- N-acetylpenicillamine (SNAP) increased outflow facility by 62 ± 28% (SD) relative to control eyes perfused with the inactive SNAP analog N-acetyl-d-penicillamine (NAP; n = 5, P = 0.016). In contrast, in eyes from eNOS-GFPtg mice, SNAP had no effect on outflow facility relative to NAP (−9 ± 4%, P = 0.40). In WT mice, the nonselective NOS inhibitor NG-nitro-l-arginine methyl ester (l-NAME, 10 μM) decreased outflow facility by 36 ± 13% ( n = 5 each, P = 0.012), but 100 μM l-NAME had no detectable effect on outflow facility (−16 ± 5%, P = 0.22). An eNOS-selective inhibitor (cavtratin, 50 μM) decreased outflow facility by 19 ± 12% in WT ( P = 0.011) and 39 ± 25% in eNOS-GFPtg ( P = 0.014) mice. In the conventional outflow pathway of eNOS-GFPtg mice, eNOS-GFP expression was localized to endothelial cells lining Schlemm's canal and the downstream vessels, with no apparent expression in the trabecular meshwork. These results suggest that endogenous NO production by eNOS within endothelial cells of Schlemm's canal or downstream vessels contributes to the physiological regulation of aqueous humor outflow facility in mice, representing a viable strategy to more successfully lower IOP in glaucoma.

Glycated collagen alters endothelial cell actin alignment and nitric oxide release in response to fluid shear stress

2011 ◽  
Vol 44 (10) ◽  
pp. 1927-1935 ◽  
Author(s):  
Steven F. Kemeny ◽  
Dannielle S. Figueroa ◽  
Allison M. Andrews ◽  
Kenneth A. Barbee ◽  
Alisa Morss Clyne
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Fluid Shear Stress ◽  
Fluid Shear ◽  
Nitric Oxide Release

Shear Stress Induces ATP-Independent Transient Nitric Oxide Release From Vascular Endothelial Cells, Measured Directly With a Porphyrinic Microsensor

1995 ◽  
Vol 77 (2) ◽  
pp. 284-293 ◽  
Author(s):  
Anthony J. Kanai ◽  
Harold C. Strauss ◽  
George A. Truskey ◽  
Anne L. Crews ◽  
Saul Grunfeld ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Nitric Oxide Release

Hydrostatic pressure and shear stress affect endothelin-1 and nitric oxide release by endothelial cells in bioreactors

2013 ◽  
Vol 9 (1) ◽  
pp. 146-154 ◽  
Author(s):  
Federico Vozzi ◽  
Francesca Bianchi ◽  
Arti Ahluwalia ◽  
Claudio Domenici
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Hydrostatic Pressure ◽  
Nitric Oxide Release ◽  
Endothelin 1

scholarly journals 17β-Estradiol Restores Endothelial Nitric Oxide Release to Shear Stress in Arterioles of Male Hypertensive Rats

Circulation ◽  
2000 ◽  
Vol 101 (1) ◽  
pp. 94-100 ◽  
Author(s):  
An Huang ◽  
Dong Sun ◽  
Akos Koller ◽  
Gabor Kaley
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Hypertensive Rats ◽  
Nitric Oxide Release ◽  
17Β Estradiol ◽  
Endothelial Nitric Oxide

scholarly journals Asymmetrical Dimethylarginine Inhibits Shear Stress–Induced Nitric Oxide Release and Dilation and Elicits Superoxide-Mediated Increase in Arteriolar Tone

Hypertension ◽  
2007 ◽  
Vol 49 (3) ◽  
pp. 563-568 ◽  
Author(s):  
Janos Toth ◽  
Anita Racz ◽  
Pawel M. Kaminski ◽  
Michael S. Wolin ◽  
Zsolt Bagi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Nitric Oxide Release ◽  
Asymmetrical Dimethylarginine ◽  
Arteriolar Tone

Role of Nitric Oxide in Buffering Short-Term Blood Pressure Fluctuations

Physiology ◽  
2000 ◽  
Vol 15 (5) ◽  
pp. 229-233 ◽  
Author(s):  
Harald M. Stauss ◽  
Pontus B. Persson
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Shear Stress ◽  
Pressure Fluctuations ◽  
Initial Increase ◽  
Short Term ◽  
Nitric Oxide Release ◽  
Arterial Blood ◽  
Endothelial Shear Stress

Blood pressure instability may promote cardiovascular morbidity. Recent data suggest a role of nitric oxide in stabilizing arterial blood pressure. A rise in blood pressure enhances endothelial shear stress and nitric oxide release. The resulting vasodilation antagonizes the initial increase in blood pressure. This system can respond within 2–10 seconds.

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