scholarly journals Cross Talk between Angiotensin II Type 1 and Type 2 Receptors: Cellular Mechanism of Angiotensin Type 2 Receptor-Mediated Cell Growth Inhibition.

1999 ◽  
Vol 22 (2) ◽  
pp. 67-74 ◽  
Author(s):  
Masatsugu Horiuchi ◽  
Meiko Hamai ◽  
Tai-Xing Cui ◽  
Masaru Iwai ◽  
Yasuhiko Minokoshi
Hypertension ◽  
2006 ◽  
Vol 47 (3) ◽  
pp. 537-544 ◽  
Author(s):  
Shetal H. Padia ◽  
Nancy L. Howell ◽  
Helmy M. Siragy ◽  
Robert M. Carey

2012 ◽  
Vol 30 ◽  
pp. e292
Author(s):  
Russell D. Brown ◽  
Rebecca Flower ◽  
Karen Moritz ◽  
Roger G Evans ◽  
Kate M. Denton

2008 ◽  
Vol 8 ◽  
pp. 434-445 ◽  
Author(s):  
Audrey Koitka ◽  
Christos Tikellis

Hypertension is now recognized as a key contributory factor to the development and progression of kidney disease in both type 1 and type 2 diabetes. The renin angiotensin system (RAS) and its effector molecule angiotensin II, in particular, have a range of hemodynamic and nonhemodynamic effects that contribute not only to the development of hypertension, but also to renal disease. As a result, therapeutic inhibition of the RAS with angiotensin-converting enzyme inhibitors and/or selective angiotensin II type 1 receptor blockers has been proposed as a key strategy for reducing kidney damage beyond the expected effects one would observe with blood pressure reduction per se. Although the relationship between the RAS and the progression of diabetic renal disease has been known for many decades, recent advances have revealed a more complex paradigm with the discovery of a number of new components. Thus, further understanding of these new components of the renin angiotensin aldosterone system (RAAS), such as the angiotensin type 2 receptor subtype, angiotensin converting enzyme 2, and the recently cloned renin receptor, is likely to have therapeutic implications for disorders such as diabetic nephropathy, where interruption of the RAAS is widely used.


2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Katrina M Mirabito ◽  
Lucinda M Hilliard ◽  
Geoffrey A Head ◽  
Robert E Widdop ◽  
Kate M Denton

2008 ◽  
Vol 22 (10) ◽  
pp. 2278-2292 ◽  
Author(s):  
Michael Grant ◽  
Haydar Alturaihi ◽  
Philippe Jaquet ◽  
Brian Collier ◽  
Ujendra Ujendra

2001 ◽  
Vol 70 (3) ◽  
pp. 265-273 ◽  
Author(s):  
Frank A. Seebach ◽  
Thomas Welte ◽  
Xin-Yuan Fu ◽  
Lutz-Henning Block ◽  
Michael Kashgarian

2012 ◽  
Vol 13 (3) ◽  
pp. 341-352 ◽  
Author(s):  
Juan Gao ◽  
Jie Chao ◽  
Karma-Jaya K Parbhu ◽  
Li Yu ◽  
Liang Xiao ◽  
...  

In the current experiment, we determined angiotensin type 2 receptor (AT2R) and angiotensin type 1 receptor (AT1R) protein expression by western blot analysis in developing normal mice. The results indicate that: (1) in all detected brain regions and in the spinal cord, adult mice exhibited significantly higher AT2R expression and lower AT1R expression in total protein extracts compared to fetuses and neonates; (2) other major organs, including heart, lung, liver and kidney, exhibited the same expression pattern as the brain and spinal cord; (3) reciprocal changes in AT2R and AT1R expression were found in the total protein extracts from the brainstems of mice from one-day prenatal to six weeks of age, and there was a negative correlation between AT2R and AT1R protein expression; (4) in both membrane and cytosolic fractions from the brainstem, adult mice exhibited higher AT2R and lower AT1R expression than did fetuses and neonates; and (5) in the brainstem, there were no significant differences in AT2R and AT1R messenger RNA (mRNA) levels among fetal, neonatal and adult mice. The above results reconfirmed our previous finding in rats that adult animals have higher AT2R and lower AT1R expression compared to fetuses and neonates. These data imply an involvement of AT1R in fetal development and of AT2R in adult function.


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