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Am J Physiol Renal Physiol (August 9, 2001). doi:10.1152/ajprenal.0335.2000
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Articles in PresS, published online ahead of print August 9, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.0335.2000
Submitted on December 12, 2000
Accepted on July 10, 2001

Intrarenal AT1 Receptor and ACE Binding in Angiotensin II-Induced Hypertensive Rats

Lisa M Harrison-Bernard1*, Jialong Zhuo2, Hiroyuki Kobori1, Mitsuru Ohishi2, and Luis G Navar1

1 Physiology, Tulane University Health Sciences Center, New Orleans, LA, USA
2 Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria, Australia

* To whom correspondence should be addressed. E-mail: lharris{at}tulane.edu.

The aim of this study was to assess differential alterations in the intrarenal expression of angiotensin II (AngII) type 1 (AT1) receptors and angiotensin converting enzyme (ACE) that may explain the augmented intrarenal AngII influence in AngII-induced hypertension. Rats were infused with 80 ng/min AngII (n=8) via osmotic minipump implanted subcutaneously for 2 wks. Control animals were subjected to sham surgery (n=7). On day 12, systolic blood pressure averaged 184±3 and 125±1 mmHg in AngII-infused compared to Sham rats (p<0.05). Total kidney AT1 receptor protein levels measured by Western blot analysis were not altered significantly. AT1 receptor binding mapped by quantitative in vitro autoradiography was significantly decreased in glomeruli (172±25 vs 275±34 dpm/mm2; p<0.05) and the inner stripe of the outer medulla (121±17 vs 178±19 dpm/mm2; p<0.05) of AngII-infused compared to Sham rats at 13 days. However, proximal convoluted tubule AT1 receptor binding was not significantly altered (48±9 vs 58±6 dpm/mm2; n=8, 7 p=0.5). ACE binding was significantly augmented (132±4 vs 97±3 dpm/mm2; n=8, 7; p<0.0001) in AngII infused rats. In summary, during AngII-induced hypertension, glomeruli and inner stripe of the outer medulla have reduced AT1 receptor binding. Proximal convoluted tubules exhibit maintained AT1 receptor density and increased ACE binding, which together with the elevated AngII levels suggests that AngII exerts a sustained influence on tubular reabsorption and consequently contributes to the development and maintenance of AngII-dependent hypertension.




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