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 hydronephrotic kidney without ischaemia, blood pressure did not change significantly. 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 increased from 81 +/- 2 to 135 +/- 6 mmHg (p < 0.01). Plasma renin increased; renin and renin mRNA levels increased significantly in the ischaemic hydronephrotic kidney (p < 0.01), but not in the contralateral kidney. Thus, the presence of the macula densa is critical for renin release but not for renin gene expression. Aortic ligation results in a significant rise in blood pressure and the activity of the RAS. The mechanisms may involve a baroreceptor and/or an unknown factor.