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1 Max Delbruck Center for Molecular Medicine, Berlin, Germany
2 Franz Volhard Clinic, HELIOS Klinikum-Berlin, Medical Faculty of the Charite, Berlin, Germany
3 Department of Cell Biology and Physiology, Washington University of Medicine, St. Louis, MO, USA
4 Autonomic Dysfunction Service, Vanderbilt University, Nashville, TN, USA
5 Max Delbruck Center for Molecular Medicine, Berlin, Germany; Franz Volhard Clinic, HELIOS Klinikum-Berlin, Medical Faculty of the Charite, Berlin, Germany
* To whom correspondence should be addressed. E-mail: vgross{at}mdc-berlin.de.
RGS2 (Regulator of G protein signaling) 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 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) was about 10 mm Hg higher in RGS2 -/- compared to RGS2 +/+ mice, while heart rate (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 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 -/- mice, compared to 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-heart rate reflex resetting, while baroreflex sensitivity remains unimpaired.
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