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1 Department of Physiology, and Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, Louisiana, United States
2 Departments of Medicine and Physiology & Biophysics, University of Iowa, Iowa City, Iowa, United States
* To whom correspondence should be addressed. E-mail: hkobori{at}tulane.edu.
This study was performed in transgenic mice to test the hypothesis that the selective intrarenal overproduction of angiotensin (Ang) II increases intrarenal mouse angiotensinogen (mAGT) expression. We utilized 3 groups: 1) single transgenic mice (A, N=14) expressing human angiotensinogen (hAGT) only in the kidney, 2) double transgenic mice (D, N=13) expressing human renin systemically in addition to hAGT only in the kidney, and 3) wild type (W, N=12) mice. Exogenous hAGT protein is inactive in A because endogenous mouse renin cannot cleave hAGT to AngI due to a high species-specificity. All mice were monitored from 12 to 18 weeks of age. Systolic blood pressure progressively increased from 116+/-5 mmHg (12 weeks) to 140+/-7 (18 weeks) in D. This increase was not observed in A or W. Intrarenal hAGT levels were similar in A and D; however, hAGT was not detectable in kidneys of W. Kidney AngII levels were increased in D (216+/-43 fmol/g) compared with A (117+/-16) and W (118+/-17). However, plasma AngII concentrations were similar among the 3 groups. Endogenous renal mAGT mRNA was significantly increased in D (1.46+/-0.19, ratio) compared with A (0.97+/-0.12) and W (1.00+/-0.08). Endogenous renal mAGT protein was also significantly increased in D compared with A and W. Interstitial collagen-positive area, interstitial macrophage/monocyte infiltration, and afferent arteriolar wall thickness were significantly increased in D compared with A and W. These data indicate for the first time that the selective stimulation of intrarenal production of AngII from hAGT augments endogenous intrarenal mAGT mRNA and protein expression.
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