Decreased perfusion pressure modulates renin and ANG II type 1 receptor gene expression in the rat kidney

To determine whether decreased perfusion pressure affects the abundance and distribution of renin and its mRNA and the expression of the angiotensin II type 1 (AT₁) receptor gene within the kidney, adult male Sprague-Dawley rats were subjected to aortic coarctation proximal to the renal arteries (Coarc, n = 8) and compared with sham-operated rats (Sham, n = 6). Renal renin distribution was determined by immunocytochemistry using a specific polyclonal antibody against rat renin. Renin mRNA was assessed by in situ hybridization to a ³⁵S-labeled oligonucleotide complementary to rat renin mRNA. Kidney AT₁ mRNA levels were determined by Northern analysis using a 1,133-base pair rat AT₁ cDNA. Femoral arterial blood pressure, measured 24 h after surgery, was lower in Coarc than in Sham rats (75 ± 5.4 vs. 122 ± 2.3 mmHg, P < 0.05). Aortic coarctation increased the percent of juxtaglomerular apparatuses (%JGA) containing renin and its mRNA (85 ± 2.5 and 66 ± 2.8 vs. 49 ± 5.3 and 36 ± 1.7%, Coarc vs. Sham, P < 0.05) and the intensity of hybridization signals (497 ± 89 vs. 71 ± 12 grains/JGA, Coarc vs. Sham, P < 0.05). In addition, recruitment of renin gene expressing cells was observed along afferent arterioles in Coarc rats, whereas renin and its mRNA were limited to the JGAs in Sham rats. Renal AT₁ receptor gene expression was threefold lower in Coarc than in Sham rats. We conclude that reduction of perfusion pressure after abdominal aortic coarctation acutely enhances renin gene expression and downregulates AT₁ receptor gene expression. We speculate that downregulation of AT₁ receptor mRNA in the presence of recruitment of renin gene expressing cells within the kidney may represent a local homeostatic mechanism to maintain renal perfusion pressure.