gms | German Medical Science

RGS2 deletion in mice prolongs signaling by G protein-coupled vasoconstrictor receptors and increases blood pressure; however, much remains unclear about blood pressure regulation in the face of RGS2 deficiency. We tested autonomic nervous system function and blood pressure regulation in RGS2-deficient mice (RGS2 -/-). We measured arterial blood pressure and heart rate with telemetry, computed time and frequency-domain measures for blood pressure and heart rate variability (HRV) as well as baroreflex sensitivity (BRS-LF), and assessed environmental stress sensitivity. Mean arterial blood pressure (MAP) increased by 10 mm Hg, while heart rate (HR) was unchanged in RGS2 -/- mice, indicating a resetting of the baroreceptor reflex. Atropine increased MAP more in RGS2 -/- than in RGS2 +/+ mice while HR responses were not different. In contrast, hexamethonium decreased HR and MAP in RGS2 +/+ and had only small effects in RGS2 -/-. Urinary norepinephrine excretion was higher in RGS2 -/- than in RGS2 +/+. Prazosin decreased blood pressure in RGS2 +/+ (D 19 ± 6 mmHg) and RGS2 -/- mice (D 28 ± 7 mmHg). The LF and HF power of HRV were reduced in RGS2 -/- compared to controls while BRS-LF and SBP-LF were not different. Atropine and atropine+metoprolol markedly reduced the HRV parameters in the time (RMSSD) and frequency domain (LF, HF, LF/HF) in both strains. Environmental stress sensitivity was increased in RGS2 -/- . We conclude that RGS2 deletion increases sympathetic tone and leads to a baroreceptor-heart rate reflex resetting, while baroreflex sensitivity remains unimpaired.