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1 Department of Physiology, Tulane University Health Sciences Center, New Orleans, Louisiana 70112; and 2 Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria 3052, Australia
The intrarenal expression of
angiotensin II (ANG II) type 1 (AT1) receptors and
angiotensin-converting enzyme (ACE) was determined in ANG II-induced
hypertensive rats (80 ng/min; 2 wk). Systolic blood pressure averaged
184 ± 3 and 125 ± 1 mmHg in ANG II-infused compared with
Sham rats on day 12. Total kidney AT1 receptor
protein levels were not altered significantly. AT1 receptor
binding mapped by quantitative in vitro autoradiography was
significantly decreased in glomeruli (172 ± 25 vs. 275 ± 34 disintegrations · min
1 · mm
2)
and the inner stripe of the outer medulla (121 ± 17 vs. 178 ± 19 disintegrations · min
1 · mm
2), but not proximal convoluted tubules (48 ± 9 vs. 58 ± 6 disintegrations · min
1 · mm
2)
of ANG II-infused compared with Sham rats. Proximal tubule ACE binding
was significantly augmented (132 ± 4 vs. 97 ± 3 disintegrations · min
1 · mm
2)
in ANG II-infused rats. In summary, during ANG II-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 ANG II levels suggest that ANG II
exerts a sustained influence on tubular reabsorption and consequently
contributes to the development and maintenance of ANG II-dependent hypertension.
Western blot analysis; glomeruli; proximal convoluted tubules; outer medulla; in vitro autoradiography; osmotic minipump
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