urinary angiotensinogen as an indicator of intrarenal angiotensin status in hypertension. Hypertension 2003;41:42–49. [PubMed: 12511528] Williams et al. Page 8 Am J Med Sci. Author manuscript; available

Abstract—Angiotensin II (AngII) infusions augment renal angiotensinogen mRNA and protein and urinary angioten-sinogen excretion (UAGT). Further experiments were performed in 4 groups of rats: normal salt diet with sham operation, NSSham, n6; NS with AngII infusion at 40 ng/min via osmotic minipump, NSAngII(40), n9; NS with AngII infusion at 80 ng/min, NSAngII(80), n9; high-salt diet with deoxycorticosterone acetate salt pellet (100 mg), HSDOCA, n4. These experiments sought to determine whether enhanced UAGT is specifically associated with increased kidney AngII levels or is a nonspecific consequence of the hypertension. Systolic BP (SBP) was significantly increased to 1312 and 1622 mm Hg at day 11 in NSAngII(40) and NSAngII(80), respectively, compared with NSSham (1101). Regression analysis demonstrated a positive relationship (R0.49) between SBP and UAGT for NSSham (1.10.3 nmol AngI/d), NSAngII(40) (2.50.9), and NSAngII(80) (5.51.5). UAGT was also highly correlated (R0.70) with kidney AngII content for NSSham (496 fmol/g), NSAngII(40) (21549), and NSAngII(80) (34747); but not with plasma AngII (R0.12). HSDOCA rats also exhibited increased SBP to 1341 mm Hg, but UAGT (1.40.4 nmol AngI/d) and intrarenal AngII content (132 fmol/g) were not increased despite the hypertension. Infused human angiotensinogen could not be detected in urine of sham-operated or AngII-infused rats (n4 each). These data demonstrate that UAGT increases in AngII-dependent hypertension in a dose- and time-dependent manner, but not in hypertension elicited by HSDOCA. The results support the hypothesis that AngII-dependen