Clonidine Improves Spontaneous Baroreflex Sensitivity in Conscious Mice Through Parasympathetic Activation

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Abstract
α-2 Adrenoceptors are important in baroreflex regulation. We tested the impact of α-2 adrenoceptors on heart rate variability (HRV) and spontaneous baroreflex sensitivity (BRS) in conscious mice with telemetry (TA11PA-C20). Baseline beat-to-beat measurements (2 hours between 8:00 am to 12:00 pm ) were compared with measurements after intraperitoneal α-2 adrenoceptor blockade (yohimbine 2 mg/kg) and α-2 adrenoceptor stimulation (clonidine 1, 10, and 50 mg/kg). Blood pressure (BP) was 128±6/87±6 mm Hg and heart rate (HR) was 548±18 bpm at baseline. BRS, calculated with the cross-spectral method, was 1.2±0.1 ms/mm Hg at baseline. BP increased 20±2/13±2 mm Hg with yohimbine. HR increased by 158±23 bpm. BRS did not change. BP decreased 16±7/5±4 mm Hg with 1 mg/kg of clonidine and did not change with a higher dose. HR decreased with clonidine (176±28, 351±21, 310±29 bpm during 1, 10, and 50 mg/kg of clonidine, P 2 during 1, 10, and 50 mg/kg of clonidine, P P <0.01). The effects of clonidine were abolished with atropine (2 mg/kg plus 50 mg/kg of clonidine) but not with metoprolol (4 mg/kg plus 50 mg/kg of clonidine). These data suggest that α-2 adrenoceptors exert a regulatory influence on autonomic cardiovascular control and baroreflex function. The effect of clonidine on baroreflex HR regulation is mediated by the parasympathetic nervous system. These murine data fit well with recent human observations regarding parasympathetic activation via α-2 adrenoceptors.