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. Author manuscript; available in PMC: 2018 Dec 1.
Published in final edited form as: Hypertension. 2017 Oct 16;70(6):1122–1131. doi: 10.1161/HYPERTENSIONAHA.117.09744

Figure 2. DOCA-salt-induced hypertension and dysautonomia are significantly attenuated in mice with B1R deletion.

Figure 2

The baseline mean arterial pressure (MAP) measured continuously by telemetry over a period of 24 hours, was similar in both wild-type (WT) control and B1R knockout (B1RKO) mice showing a clear diurnal variation (A, n=6–12). Deoxycorticosterone acetate (DOCA) implanted subcutaneously and combined with 1% salt as drinking solution induced a progressive rise of MAP in sham-treated controls that was attenuated in B1RKO mice (B, n=8 mice/group, Repeated measures two-way ANOVA, *P<0.01 vs. Sham, †P<0.05 vs. WT+DOCA). After 21 days of DOCA-salt treatment, autonomic function was assessed pharmacologically by determining the changes in MAP (△MAP) and heart rate (△HR) following ip injections of a β-blocker (propranolol: 4 mg/kg, Cardiac sympathetic tone, C), ganglionic blocker (chlorisondamine: 5 mg/kg, vascular sympathetic tone, D) and muscarinic antagonist (atropine: 1 mg/kg, cardiac parasympathetic tone, E). Spontaneous Baroreceptor Reflex Sensitivity (SBRS) was calculated using the sequence method (F) was improved in B1RKO mice treated with DOCA compared to WT mice. n=6–8/group. Data are presented as mean ±SEM. Two-way ANOVA, *P<0.01 vs. Sham, †P<0.01 vs. WT+DOCA.