Effects of aortic ligation on the renin angiotensin system in hydronephrotic mice

A model of aortic ligation in mice with a hydronephrotic kidney (absence of macula densa) was used to determine the effects of aortic ligation on the renal renin-angiotensin system (RAS). Blood pressure increased from 83 +/- 2 to 133 +/- 8 mmHg within 7 days after aortic ligation (p < 0.01). Aortic ligation increased plasma renin (p < 0.01); renin (p < 0.05) and renin mRNA levels (p < 0.001) rose in the ischaemic kidney. In mice with a left hydro nephrotic kidney without ischaemia, blood pressure did not change significa ntly. Plasma renin levels from the left renal vein were lower than from the contralateral vein, but renin (p < 0.01) and renin mRNA levels (p < 0.05) in the hydronephrotic kidney were higher than in the contralateral kidney. In mice with hydronephrosis that had an aortic ligature, blood pressure inc reased from 81 +/- 2 to 135 +/- 6 mmHg (p < 0.01). Plasma renin increased; renin and renin mRNA levels increased significantly in the ischaemic hydron ephrotic kidney (n < 0.01), but not in the contralateral kidney. Thus, the presence of the macula densa is critical for renin release but not for reni n gene expression. Aortic ligation results in a significant rise in blood p ressure and the activity of the RAS. The mechanisms may involve a barorecep tor and/or an unknown factor.