Increased nitric oxide formation followed by increased arginase activity induces relative lack of arginine at the wound site and alters whole nutritional status in rats almost within the early healing period

Nitric Oxide ◽  
2009 ◽  
Vol 20 (4) ◽  
pp. 253-258 ◽  
Author(s):  
Gordana Žunić ◽  
Gordana Šupić ◽  
Zvonko Magić ◽  
Biljana Drašković ◽  
Milijana Vasiljevska
Keyword(s):  
Nitric Oxide ◽  
Nutritional Status ◽  
Arginase Activity ◽  
Oxide Formation ◽  
Wound Site ◽  
Relative Lack ◽  
Nitric Oxide Formation ◽  
Healing Period ◽  
Early Healing

Arginase inhibition restores arteriolar endothelial function in Dahl rats with salt-induced hypertension

2005 ◽  
Vol 288 (4) ◽  
pp. R1057-R1062 ◽  
Author(s):  
Fruzsina K. Johnson ◽  
Robert A. Johnson ◽  
Kelly J. Peyton ◽  
William Durante
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
High Salt ◽  
Arginase Activity ◽  
Oxide Formation ◽  
Nitric Oxide Formation ◽  
Arterial Blood ◽  
Low Salt ◽  
Induced Hypertension ◽  
Luminal Flow

Vascular tissues express arginase that metabolizes l-arginine to l-ornithine and urea and thus reduces substrate availability for nitric oxide formation. Dahl salt-sensitive (Dahl-S) rats with salt-induced hypertension show endothelial dysfunction, including decreased vascular nitric oxide formation. This study tests the hypothesis that increased vascular arginase activity contributes to endothelial dysfunction in hypertensive Dahl-S rats. Male Dahl-S rats (5–6 wk) were placed on high (8%) or low (0.3%) NaCl diets for 4 wk. With respect to the low-salt group, mean arterial blood pressure was increased in the high-salt animals. Immunohistochemical stainings for arginase I and II were enhanced in arterioles isolated from high-salt Dahl-S rats. Experiments used isolated Krebs buffer-superfused first-order gracilis muscle arterioles with constant pressure (80 mmHg) and no luminal flow or constant midpoint but altered endpoint pressures to establish graded levels of luminal flow (0–50 μl/min). In high-salt arterioles, responses to an endothelium-dependent vasodilator acetylcholine (1 nmol/l to 3 μmol/l) and flow-induced dilation were decreased. Acute in vitro treatment with an inhibitor of arginase, 100 μmol/l ( S)-(2-boronoethyl)-l-cystine, or the nitric oxide precursor, 1 mmol/l l-arginine, similarly enhanced acetylcholine and flow-induced maximal dilations and abolished the differences between high- and low-salt arterioles. These data show that arteriolar arginase expression is increased and that endothelium-dependent vasodilation is decreased in high-salt Dahl-S rats. Acute pretreatment with an arginase inhibitor or with l-arginine restores endothelium-dependent vasodilation and abolishes the differences between high- and low-salt groups. These results suggest that enhanced vascular arginase activity contributes to endothelial dysfunction in Dahl-S rats with salt-induced hypertension and identifies arginase as a potential therapeutic target to prevent endothelial dysfunction.

Aminoguanidine, a novel inhibitor of nitric oxide formation, prevents diabetic vascular dysfunction

Diabetes ◽  
1992 ◽  
Vol 41 (4) ◽  
pp. 552-556 ◽  
Author(s):  
J. A. Corbett ◽  
R. G. Tilton ◽  
K. Chang ◽  
K. S. Hasan ◽  
Y. Ido ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Dysfunction ◽  
Oxide Formation ◽  
Nitric Oxide Formation

scholarly journals Nitric oxide formation during light-induced decomposition of phenyl N-tert-butylnitrone

1993 ◽  
Vol 268 (16) ◽  
pp. 11520-11527
Author(s):  
W. Chamulitrat ◽  
S.J. Jordan ◽  
R.P. Mason ◽  
K. Saito ◽  
R.G. Cutler
Keyword(s):  
Nitric Oxide ◽  
Oxide Formation ◽  
Nitric Oxide Formation ◽  
Induced Decomposition

scholarly journals Zinc regulates iNOS-derived nitric oxide formation in endothelial cells

Redox Biology ◽  
2014 ◽  
Vol 2 ◽  
pp. 945-954 ◽  
Author(s):  
Miriam M. Cortese-Krott ◽  
Larissa Kulakov ◽  
Christian Opländer ◽  
Victoria Kolb-Bachofen ◽  
Klaus-D. Kröncke ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Oxide Formation ◽  
Nitric Oxide Formation

Room F, 10/17/2000 9: 00 AM - 11: 00 AM (PS) Interleukin-10 Inhibits Nitric Oxide Formation in Murine Macrophages by Suppressing CAT-2 Transcription 

2000 ◽  
Vol 93 (3A) ◽  
pp. A-451
Author(s):  
Chun-Jen Huang ◽  
R. B. Nielsen ◽  
David R. Nelson ◽  
Bruce R. Stevens ◽  
Jeffrey W. Skimming
Keyword(s):  
Nitric Oxide ◽  
Interleukin 10 ◽  
Oxide Formation ◽  
Murine Macrophages ◽  
Nitric Oxide Formation
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