scholarly journals Renin-Angiotensin System and Nitric Oxide Synthase Gene Polymorphisms in Relation to Stroke

2007 ◽  
Vol 20 (7) ◽  
pp. 764-770 ◽  
Author(s):  
L HENSKENS ◽  
A KROON ◽  
Y VANDERSCHOUW ◽  
P SCHIFFERS ◽  
D GROBBEE ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Gene Polymorphisms ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Oxide Synthase

Nitric Oxide Synthase and Renin-Angiotensin System Gene Expression in Salt-Sensitive and Salt-Resistant Sabra Rats

Hypertension ◽  
1997 ◽  
Vol 30 (3) ◽  
pp. 409-415 ◽  
Author(s):  
Andrea Lippoldt ◽  
Volkmar Gross ◽  
Kerstin Schneider ◽  
Anita Hansson ◽  
Sophie Nadaud ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Oxide Synthase

Synergistic effect of renin-angiotensin system and nitric oxide synthase genes polymorphisms in pre-eclampsia

2007 ◽  
Vol 86 (6) ◽  
pp. 678-682 ◽  
Author(s):  
Chiara Benedetto ◽  
Luca Marozio ◽  
Giovannino Ciccone ◽  
Giuseppina Chieppa ◽  
Marco Quaglia ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Synergistic Effect ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Oxide Synthase

scholarly journals Locally Activated Renin-Angiotensin System Associated with TGF-β1 as a Major Factor for Renal Injury Induced by Chronic Inhibition of Nitric Oxide Synthase in Rats

2000 ◽  
Vol 11 (4) ◽  
pp. 616-624 ◽  
Author(s):  
MINORU KASHIWAGI ◽  
MICHIYA SHINOZAKI ◽  
HIDEKI HIRAKATA ◽  
KIYOSHI TAMAKI ◽  
TADASHI HIRANO ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Renal Injury ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Oxide Synthase ◽  
Tgf Β1

Abstract. Chronic inhibition of nitric oxide synthase (NOS) is known to cause renal parenchymal injury with systemic hypertension. To elucidate the pathogenetic mechanism in renal damage induced by NOS inhibition,Nω-nitro-L-arginine methyl ester (L-NAME) was given orally for 12 wk in Wistar rats, and the roles of tissue renin-angiotensin system and transforming growth factor-β1 (TGF-β1) were investigated. BP and urinary protein excretion increased significantly in L-NAME rats compared with control rats, and glomerulosclerosis and interstitial fibrosis developed. In L-NAME rats, the cortical tissue levels of angiotensin-converting enzyme activity and angiotensin II were significantly higher than those in control rats. The cortical mRNA expressions of both TGF-β1 and fibronectin were significantly elevated in L-NAME rats. Immunohistochemically, increased expressions of both fibronectin and α-smooth muscle actin were also revealed in L-NAME rats. In L-NAME rats, these histologic injuries and the increased expression of TGF-β1 were equally emeliorated by either angiotensin-converting enzyme inhibitor or angiotensin II type 1 receptor antagonist, but not by hydralazine. In conclusion, the locally activated renin-angiotensin system in connection with the increased TGF-β1 expression is a major pathogenetic feature of renal injury in chronically NOS-inhibited rats.

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