Angiotensin II Receptor Blockade Ameliorates Mesangioproliferative Glomerulonephritis in Rats through Suppression of CTGF and PAI-1, Independently of the Coagulation System

2007 ◽  
Vol 105 (3) ◽  
pp. e65-e74 ◽  
Author(s):  
Ning Liu ◽  
Shinya Shimizu ◽  
Toshiko Ito-Ihara ◽  
Kuniaki Takagi ◽  
Toru Kita ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Coagulation System ◽  
Receptor Blockade ◽  
Angiotensin Ii Receptor ◽  
Mesangioproliferative Glomerulonephritis ◽  
Angiotensin Ii Receptor Blockade ◽  
Pai 1

Late angiotensin II receptor blockade in progressive rat mesangioproliferative glomerulonephritis: new insights into mechanisms

2013 ◽  
Vol 229 (5) ◽  
pp. 672-684 ◽  
Author(s):  
Luigi Villa ◽  
Peter Boor ◽  
Andrzej Konieczny ◽  
Uta Kunter ◽  
Claudia RC van Roeyen ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Blockade ◽  
Angiotensin Ii Receptor ◽  
Mesangioproliferative Glomerulonephritis ◽  
Angiotensin Ii Receptor Blockade

scholarly journals Angiotensin II receptor blockade and insulin sensitivity in overweight and obese adults with elevated blood pressure

2013 ◽  
Vol 7 (1) ◽  
pp. 11-20 ◽  
Author(s):  
Elaina L. Marinik ◽  
Madlyn I. Frisard ◽  
Matthew W. Hulver ◽  
Brenda M. Davy ◽  
Jose M. Rivero ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Insulin Sensitivity ◽  
Angiotensin Ii ◽  
Elevated Blood Pressure ◽  
Receptor Blockade ◽  
Elevated Blood ◽  
Angiotensin Ii Receptor ◽  
Obese Adults ◽  
Angiotensin Ii Receptor Blockade

scholarly journals Angiotensin II receptor blockade and skeletal muscle metabolism in overweight and obese adults with elevated blood pressure

2015 ◽  
Vol 9 (2) ◽  
pp. 45-50 ◽  
Author(s):  
Nabil E. Boutagy ◽  
Elaina L. Marinik ◽  
Ryan P. McMillan ◽  
Angela S. Anderson ◽  
Madlyn I. Frisard ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Angiotensin Ii ◽  
Muscle Metabolism ◽  
Receptor Blockade ◽  
Elevated Blood ◽  
Angiotensin Ii Receptor ◽  
Obese Adults ◽  
Skeletal Muscle Metabolism ◽  
Angiotensin Ii Receptor Blockade

Experimental Diabetes Is Associated With Functional Activation of Protein Kinase Cε and Phosphorylation of Troponin I in the Heart, Which Are Prevented by Angiotensin II Receptor Blockade

1997 ◽  
Vol 81 (6) ◽  
pp. 1027-1033 ◽  
Author(s):  
Ashwani Malhotra ◽  
David Reich ◽  
Daniel Reich ◽  
Antonio Nakouzi ◽  
Vinay Sanghi ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Protein Kinase ◽  
Troponin I ◽  
Experimental Diabetes ◽  
Receptor Blockade ◽  
Angiotensin Ii Receptor ◽  
Angiotensin Ii Receptor Blockade

scholarly journals Angiotensin II receptor blockade blocker pre-treatment largely prevents injury from gradual renal ablation in rats

2007 ◽  
Vol 8 (3) ◽  
pp. 110-117 ◽  
Author(s):  
Hye Won Park ◽  
Youngki Kim ◽  
Kee Hyuck Kim ◽  
Hyeon Joo Jeong ◽  
Myung-Hee Shin ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Blockade ◽  
Angiotensin Ii Receptor ◽  
Renal Ablation ◽  
Pre Treatment ◽  
Angiotensin Ii Receptor Blockade

Angiotensin II/Angiotensin II Receptor Blockade Affects Osteoporosis via the AT1/AT2-Mediated cAMP-Dependent PKA Pathway

2017 ◽  
Vol 204 (1) ◽  
pp. 25-37 ◽  
Author(s):  
Yi Zhou ◽  
Xiaoxu Guan ◽  
Xiaoyi Chen ◽  
Mengfei Yu ◽  
Chaowei Wang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Bone Mass ◽  
Animal Studies ◽  
Underlying Mechanism ◽  
Receptor Blockade ◽  
Angiotensin Ii Receptor ◽  
Matrix Mineralization ◽  
Angiotensin Ii Receptor Blockade ◽  
Pka Pathway

Animal studies have reported on the benefits of ARB on bone mass. However, the underlying mechanism for angiotensin II (AngII)/AngII receptor blockade (ARB) in regulating bone mass remains elusive. Since high levels of plasma and urine cAMP are observed in osteoporotic and hypertensive patients, we hypothesized that cAMP may be an important molecule for the downstream events of the activation of AT receptors, members of the G-protein-coupled receptor family, in regulating bone turnover. In this study, micro-CT and X-ray analyses indicated that AngII decreased bone mass via biasing bone resorption over bone formation in osteoporotic mice. However, these adverse effects were blocked by olmesartan and PD123319. In vitro, AngII was shown to downregulate osteogenic differentiation and matrix mineralization, but to upregulate osteoclastic activity by mainly affecting osteoblasts producing osteoclastogenesis-associated key soluble factors, including M-CSF and RANKL. Similarly, ARB treatment exhibited antagonistic effects on AngII. In conclusion, osteoblasts are the directly targeted cells. ARB1 exhibits a greater capacity to increase bone mass than ARB2. The cAMP-dependent PKA pathway plays an important role in AngII/ARB on changing bone mass.

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