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 ren in-angiotensin system (RAS), since the obstructed kidney increases ren in secretion (Ref 8). In an attempt to delineate the role of the RAS i n this hypertensive model, we acutely obstructed the ureter in two gro ups of dogs that previous to the obstruction received either placebo ( G I, n = 8) or 50 mg of captopril, an angiotensin-converting enzyme in hibitor (G II, n = 9). Animals that received placebo showed a consiste nt increase in mean arterial pressure (MAP), 128 +/- 4 vs. 144 +/- 4 m m Hg (p <0.001); those that received captopril did not show such a ten dency: 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 me asured; Group IV (G IV, n = 5), identical to G II except that they rec eived 50 mg of indomethacin, 60 min before captopril; and group V (G V n = 6), which was sham operated and measured for PRA and ALDO. MAP, P RA, 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 Al/ mL/h (p <0.001); and 41 +/- 18 vs. 144 +/- 25 pg/mL (p <0.01); meanwhi le MAP of G IV and G V was not modified: 128 +/- 17 vs. 12 7 +/- 17 an d 133 +/- 8 vs. 136 +/- 7 mm Hg, respectively; PRA and ALDO were not c hanged 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 an imals that were not pharmacologically manipulated exhibited an increas e in MAP during AUUO (G I and G III), and because such an elevation wa s associated to an increase in PRA and ALDO (G III), we suggest art ac tivation of the RAS in the genesis of this particular model of arteria l hypertension.