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1 Department of Physiology, SL39, Tulane University School of Medicine, New Orleans,, Louisiana, United States; Division of Natural Sciences, University of California, Merced, California, United States
2 Department of Physiology, SL39, Tulane University School of Medicine, New Orleans,, Louisiana, United States
3 Department of Physiology, SL39, Tulane University School of Medicine, New Orleans,, Louisiana, United States; Physiology and Biophysics, State University of New York at Buffalo, Buffalo, New York, United States
* To whom correspondence should be addressed. E-mail: rortiz{at}ucmerced.edu.
Effects of aldosterone receptor (AR) blockade on renal Na+ excretion, arterial blood pressure, and intra-adrenal and renal Ang II levels during Ang II-dependent hypertension were evaluated. Rats from one cohort (n = 10/group; 1) control, 2) control + eplerenone (epl; 25 mg/d), 3) Ang II (60 ng/min), and 4) Ang II + epl) were maintained in metabolic cages (28 d) for daily urine collections. Systolic blood pressure (SBP) was measured weekly by tail-cuff. In a second cohort (n=12/group), daily SBP was measured by telemetry (n=6 rats/group; 1) control, 2) Ang II, and 3) Ang II + epl). A diet containing epl (0.1 %) was provided after 1 week of Ang II infusion. Direct monitoring of BP by telemetry showed that epl delayed the onset of the increase in SBP by 2 days and slightly reduced SBP (186 ± 6 vs 177 ± 8 mmHg). Epl transiently increased Na+ excretion within 24 hr of treatment in both normo- and hypertensive rats, but cortical 
ENaC content was not altered after 21 days of Epl treatment. Epl exacerbated the Ang II mediated increases in intrarenal (226 ± 16 vs 365 ± 38 fmol/g) and intra-adrenal Ang II (3.9 ± 0.3 vs 8.2 ± 0.9 fmol/mg) content. Exacerbation of intrarenal Ang II levels likely contributes to the maintenance of ENaC protein content, and thus Na+ reabsorption, which helps explain the ineffectiveness of AR blockade in reducing SBP in Ang II-infused models of hypertension.
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