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. Author manuscript; available in PMC: 2011 Nov 3.
Published in final edited form as: Cell Metab. 2010 Nov 3;12(5):431–442. doi: 10.1016/j.cmet.2010.09.011

Figure 5. Suppression of the peripheral RAS contributes to the metabolic phenotypes of sRA mice.

Figure 5

(A) Angiotensin II in whole-brain homogenate (Control N=5, sRA N=7), cortex (Control N=4, sRA N=4), combined anteroventral third ventricle (AV3V) and hypothalamic regions (Control N=4, sRA N=3), and brain stem (Control N=4, sRA N=3). (B) Plasma RAS peptides (N=8 for all). (C) Renal murine renin mRNA expression (N=4 for all). (D) Mean arterial blood pressure determined by carotid artery cannula during anesthesia (Control N=7, sRA N=6), and in conscious, freely-moving mice by radiotelemetry during dark and light phases (Control N=4, sRA N=4). (E) Metabolic rate and respiratory quotient following angiotensin II treatment (100 ng/kg/min, s.c., for 8 weeks. Males only; Control saline, Ang II N=4 each. sRA saline N=7, sRA Ang II N=3). * P<0.05 vs. control. † P≤0.05 vs. saline-treated sRA. All data are mean ± SEM.