Role of the Renin—Angiotensin System in Arterial Hypertension Secondary to Acute Unilateral Urinary Obstruction

Acute unilateral ureteral obstruction (AUUO) has been associated to a blood pressure increase, presumably secondary to activation of the reninangiotensin system (RAS), since the obstructed kidney increases renin secretion (Ref. 8). In an attempt to delineate the role of the RAS in this hypertensive model, we acutely obstructed the ureter in two groups of dogs that previous to the obstruction received either placebo (G 1, n = 8) or 50 mg of captopril, an angiotensin-converting enzyme inhibitor (G II, n = 9). Animals that received placebo showed a consistent increase in mean arterial pressure (MAP), 128 ± 4 vs. 144 ± 4 mm Hg (p < 0.001); those that received captopril did not show such a tendency: 135 ± 7 vs. 135 ± 7 mm Hg. In further studies, three groups of animals were included: group III (G III, n = 4), identical to G I except that plasma renin activity (PRA) and aldosterone (ALDO) were measured; Group IV (G IV, n = 5), identical to G II except that they received 50 mg of indomethacin, 60 min before captopril; and group V (G V, n = 6), which was sham operated and measured for PRA rind ALDO. MAP, PRA, and ALDO showed a consistent tendency to increase in G III: 141 ± 5 vs. 160±8 mm Hg (p < 0.05); 0.89±0.3 vs.4.4 ± 0.9 ng AI/mL/h (p < 0.001); and 41±18 vs. 144 ± 25 pg/mL (p < 0.01); meanwhile MAP of G IV and G V was not modified: 128 ± 17 vs. 127 ± 17 and 133 ± 8 vs. 136 ± 7 mm Hg, respectively; PRA and ALDO were not changed either, in the latter group: 1.9 ± 1.2 vs. 2.1 ± 1.7 ng AI/mL/h and 64 ± 22 vs. 91 ± 50 pg/mL, respectively. Because those animals that were not pharmacologically manipulated exhibited an increase in MAP during AUUO (G I and G III), and because such an elevation was associated to an increase in PRA and ALDO (G III), we suggcst an activation of the RAS in the genesis of this particular model of arterial hypertension.