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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 1. Mice with brain renin-angiotensin system hyperactivity (sRA mice) exhibit potent hydromineral phenotypes.

Figure 1

(A) Ad libitum 24-hour intake volumes for tap water and 0.15 M NaCl solutions (Control N=6, sRA N=3). (B) NaCl preference, total fluid intake, total sodium intake, urine volume, urine sodium concentration (UNaC), and urine osmolality from sRA and control littermate mice offered ad libitum access to varying concentrations of NaCl drink solution, distilled water, and standard chow (Control N=6, sRA N=6). (C) Renal sympathetic nerve activity (RSNA) (Males only; Control N=7, sRA N=6). (D) Blood hematocrit (Control N=9, sRA N=8). (E) Serum osmolality (Control N=10, sRA N=6), potassium concentration, and sodium concentration (Control N=17, sRA N=15). (F) Analysis of pup survival to birth and to weaning. (G) Plasma arginine vasopressin (AVP) concentrations at baseline and following a 4-hour water restriction (N=4 for all). (H) Total 24-hour sodium intake, preference for 0.15 M NaCl, fluid intake and urine volume after treatment with conivaptan (Saline N=5, Conivaptan N=6). * P<0.05 vs. control, or sRA+Saline. All data are mean ± SEM. See also Figure S1.