Blockade of nitric oxide formation inhibits the stimulation of the renin system by a low salt intake

1996 ◽  
Vol 432 (2) ◽  
pp. 187-191 ◽  
Author(s):  
Karin Schricker ◽  
Armin Kurtz
Keyword(s):  
Nitric Oxide ◽  
Salt Intake ◽  
Oxide Formation ◽  
Nitric Oxide Formation ◽  
Low Salt ◽  
Stimulation Of

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
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