A. Tufromcreddie et al., DECREASED PERFUSION-PRESSURE MODULATES RENIN AND ANG-II TYPE-1 RECEPTOR GENE-EXPRESSION IN THE RAT-KIDNEY, The American journal of physiology, 264(4), 1993, pp. 696-702
To determine whether decreased perfusion pressure affects the abundanc
e and distribution of renin and its mRNA and the expression of the ang
iotensin II type 1 (AT1) receptor gene within the kidney, adult male S
prague-Dawley rats were subjected to aortic coarctation proximal to th
e renal arteries (Coarc, n = 8) and compared with sham-operated rats (
Sham, n = 6). Renal renin distribution was determined by immunocytoche
mistry using a specific polyclonal antibody against rat renin. Renin m
RNA was assessed by in situ hybridization to a S-35-labeled oligonucle
otide complementary to rat renin mRNA. Kidney AT1 mRNA levels were det
ermined by Northern analysis using a 1,133-base pair rat AT1 cDNA. Fem
oral arterial blood pressure, measured 24 h after surgery, was lower i
n Coarc than in Sham rats (75 +/- 5.4 vs. 122 +/- 2.3 mmHg, P < 0.05).
Aortic coarctation increased the percent of juxtaglomerular apparatus
es (%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 intensi
ty of hybridization signals (497 +/- 89 vs. 71 +/- 12 grains/JGA, Coar
c vs. Sham, P < 0.05). In addition, recruitment of renin gene expressi
ng cells was observed along afferent arterioles in Coarc rats, whereas
renin and its mRNA were limited to the JGAs in Sham rats. Renal AT1 r
eceptor gene expression was threefold lower in Coarc than in Sham rats
. We conclude that reduction of perfusion pressure after abdominal aor
tic coarctation acutely enhances renin gene expression and downregulat
es AT1 receptor gene expression. We speculate that downregulation of A
T1 receptor mRNA in the presence of recruitment of renin gene expressi
ng cells within the kidney may represent a local homeostatic mechanism
to maintain renal perfusion pressure.