Transgenic amplification of glucocorticoid action in adipose tissue causes high blood pressure in mice
J. Clin. Invest. Hiroaki Masuzaki, et al. 112:83 doi:10.1172/JCI17845 [Go to this article.]

Figure 1
(a) Daily profile of MAP in aP2-HSD1 mice at 23 weeks of age. MAP was monitored closely by telemetry transmitters implanted in the left carotid artery. Values are expressed as mean ± SEM of 60 data points each hour. Throughout the day, MAP in Tg mice (n = 17, filled squares) was significantly elevated (by 10–30 mmHg, P < 0.04) compared with that of non-Tg mice (n = 14, open circles). (b) In situ hybridization analysis of adrenal glands from aP2-HSD1 mice. Adrenal gland tissue from non-Tg (n = 5) and Tg mice (n = 3) was hybridized with ³⁵S-labeled cRNA probes for aldosterone synthetase and 11β-hydroxylase. Images of five or six sections from each gland were quantified and statistically evaluated (d). Results are expressed as arbitrary units. The ratio of aldosterone synthetase to 11β-hydroxylase (Aldo/11β) in each sample was also determined. *P < 0.02 versus non-Tg. (c) Effect of specific AT-1 receptor antagonist GA0113 on MAP in aP2-HSD1 mice at 27 weeks of age. GA0113 was administered orally once per day (0.1 mg/kg body weight, at 1500 hours) for 4 days, and the effect of drug administration was evaluated by telemetry on day 5. Filled circles, non-Tg (n = 5) initial (untreated) values; open circles, non-Tg treated; filled squares, Tg (n = 6) initial (untreated); open squares, Tg treated. *P < 0.05 vs. Tg untreated. Telemetry monitoring was continued for 4 days after the final administration to observe that MAP in both sets of mice returned to initial values.