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GENETICALLY MODIFIED ANIMALS AND MODEL ORGANISMS
1Max Delbrück Center for Molecular Medicine, Berlin; and 2Medical Faculty of the Charité, Franz Volhard Clinic, HELIOS Klinikum-Berlin, Berlin, Germany; 3Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri; and 4Autonomic Dysfunction Service, Vanderbilt University, Nashville, Tennessee
Submitted 13 April 2004 ; accepted in final form 4 January 2005
Regulator of G protein signaling (RGS2) deletion in mice prolongs signaling by G protein-coupled vasoconstrictor receptors and increases blood pressure. However, the exact mechanism of the increase in blood pressure is unknown. To address this question we tested autonomic nervous system function and blood pressure regulation in RGS2-deficient mice (RGS2 –/–). We measured arterial blood pressure and heart rate (HR) with telemetry, computed time and frequency-domain measures for blood pressure and HR variability (HRV) as well as baroreflex sensitivity [BRS-low frequency (LF)], and assessed environmental stress sensitivity. Mean arterial blood pressure (MAP) was 
10 mmHg higher in RGS2 –/– compared with RGS2 +/+ mice, while HR was not different between the groups, indicating a resetting of the baroreceptor reflex. Atropine increased MAP more in RGS2 –/– than in RGS2 +/+ mice while HR responses were not different. Urinary norepinephrine excretion was higher in RGS2 –/– than in RGS2 +/+ mice. The blood pressure decrease following prazosin was more pronounced in RGS2 –/– mice than in RGS2 +/+ mice. The LF and high-frequency (HF) power of HRV were reduced in RGS2 –/– compared with 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 –/– mice compared with controls. We conclude that the increase in blood pressure in RGS2 –/– mice is not solely explained by peripheral vascular mechanisms. A central nervous system mechanism might be implicated by an increased sympathetic tone. This state of affairs could lead to a baroreceptor-HR reflex resetting, while BRS remains unimpaired.
G protein-coupled receptors; RGS2-deficient mice; autonomic nervous system; heart rate variability; spectral analysis; baroreflex; telemetry
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