A single nucleotide mutation in the mouse renin promoter disrupts blood pressure regulation
J. Clin. Invest. Keiji Tanimoto, et al. 118:1006 doi:10.1172/JCI33824 [Go to this article.]

Figure 4
Effects of physiologic stimuli on renin gene expression in WT and TgM. (A) Renin mRNA expression in the WT CNRE and mut CNRE TgM treated with high-sodium diet (HS) or dehydration (DH). Two groups of male TgM (8-week-old) were fed high-sodium (8%) or normal-sodium (0.6%; C for control) diets for 5 days. In another group, access to drinking water was restricted for 1 day (DH). RNA was isolated from the kidney and analyzed by semiquantitative RT-PCR using 2 sets of primer pairs, one coamplifying Tg Ren-1^C (Tg) and endogenous Ren-2 and Ren-1^D (endo.) genes and another specific for the Gapdh gene (top). Relative amount of renin mRNA after normalization to that of Gapdh was determined by 3 independent RT-PCR for 3 individuals in each group (bottom). Expression value of untreated control animals in each group was arbitrarily set at 100. (B and C) Renin mRNA expression in the TgM treated with or without captopril. Six pairs each of WT and mut TgM (8-week-old) were used in the study. One group was treated for 7 days with captopril dissolved in drinking water (0.5 mg/ml). Kidneys were isolated, and RNA was analyzed as described in A. Lines in B and C indicate that lanes were run on the same gel but were noncontiguous. *P < 0.05; **P < 0.01.