Angiotensin II, oxidative stress and stem cell therapy: a matter of delicacy

2015 ◽  
Vol 128 (11) ◽  
pp. 749-750 ◽  
Author(s):  
Anton J.M. Roks
Keyword(s):  
Stem Cell ◽  
Angiotensin Ii ◽  
Cell Therapy ◽  
Stem Cell Therapy ◽  
Renal Injury ◽  
Renin Angiotensin System ◽  
Oxygen Species ◽  
Angiotensin System ◽  
Cell Donor ◽  
Ros Formation

Optimization of stem cell therapy after cardiovascular and renal injury depends on many factors, among which is stem cell donor health. The renin–angiotensin system (RAS) plays an important role in cardiovascular and renal homoeostasis and pathophysiology. It is becoming increasingly clear that the RAS affects the therapeutic performance of stem cells. In this issue of Clinical Science, Kankuri et al. dig deeper into the consequences of excessive angiotensin II signalling and reactive oxygen species (ROS) formation in the stem cell donor, applying a model of regenerative medicine after renal injury.

scholarly journals Activation of the renin-angiotensin system by a low-salt diet does not augment intratubular angiotensinogen and angiotensin II in rats

2013 ◽  
Vol 304 (5) ◽  
pp. F505-F514 ◽  
Author(s):  
Weijian Shao ◽  
Dale M. Seth ◽  
Minolfa C. Prieto ◽  
Hiroyuki Kobori ◽  
L. Gabriel Navar
Keyword(s):  
Angiotensin Ii ◽  
Renal Injury ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Angiotensin System ◽  
Salt Diet ◽  
Low Salt ◽  
Renin Mrna ◽  
Excretion Rates ◽  
Stimulation Of

In angiotensin II (ANG II) infusion hypertension, there is an augmentation of intratubular angiotensinogen (AGT) and ANG II leading to increased urinary AGT and ANG II excretion rates associated with tissue injury. However, the changes in urinary AGT and ANG II excretion rates and markers of renal injury during physiologically induced stimulation of the renin-angiotensin system (RAS) by a low-salt diet remain unclear. Male Sprague-Dawley rats received a low-salt diet (0.03% NaCl; n = 6) and normal-salt diet (0.3% NaCl, n = 6) for 13 days. Low-salt diet rats had markedly higher plasma renin activity and plasma ANG II levels. Kidney cortex renin mRNA, kidney AGT mRNA, and AGT immunoreactivity were not different; however, medullary renin mRNA, kidney renin content, and kidney ANG II levels were significantly elevated by the low-salt diet. Kidney renin immunoreactivity was also markedly increased in juxtaglomerular apparati and in cortical and medullary collecting ducts. Urinary AGT excretion rates and urinary ANG II excretion rates were not augmented by the low-salt diet. The low-salt diet caused mild renal fibrosis in glomeruli and the tubulointerstitium, but no other signs of kidney injury were evident. These results indicate that, in contrast to the response in ANG II infusion hypertension, the elevated plasma and intrarenal ANG II levels caused by physiological stimulation of RAS are not reflected by increased urinary AGT or ANG II excretion rates or the development of renal injury.

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.

scholarly journals Role of angiotensin II in stem cell therapy of cardiac disease

2015 ◽  
Vol 16 (4) ◽  
pp. 702-711 ◽  
Author(s):  
Elham Ahmadian ◽  
Samira Jafari ◽  
Ahmad Yari Khosroushahi
Keyword(s):  
Stem Cell ◽  
Angiotensin Ii ◽  
Cell Therapy ◽  
Stem Cell Therapy ◽  
Cardiac Disease
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