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NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION
1Max Delbrück Center for Molecular Medicine, Berlin; 2Medical Faculty of the Charité, Franz Volhard Clinic, HELIOS Klinikum-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 22 April 2005 ; accepted in final form 26 October 2005
The regulator of G protein signaling (RGS) 2, a GTPase-activating protein, is activated via the nitric oxide (NO)-cGMP pathway and thereby may influence blood pressure regulation. To test that notion, we measured mean arterial blood pressure (MAP) and heart rate (HR) with telemetry in N
-nitro-L-arginine methyl ester (L-NAME, 5 mg L-NAME/10 ml tap water)-treated RGS2-deficient (RGS2–/–) and RGS2-sufficient (RGS2+/+) mice and assessed autonomic function. Without L-NAME, RGS2–/– mice showed during day and night a similar increase of MAP compared with controls. L-NAME treatment increased MAP in both strains. nNOS is involved in this L-NAME-dependent blood pressure increase, since 7-nitroindazole increased MAP by 8 and 9 mmHg (P < 0.05) in both strains. The L-NAME-induced MAP increase of 14–15 mmHg during night was similar in both strains. However, the L-NAME-induced MAP increase during the day was smaller in RGS2–/– than in RGS2+/+ (11 ± 1 vs. 17 ± 2 mmHg; P < 0.05). Urinary norepinephrine and epinephrine excretion was higher in RGS2–/– than in RGS2+/+ mice. The MAP decrease after prazosin was more pronounced in L-NAME-RGS2–/–. HR variability parameters [root mean square of successive differences (RMSSD), low-frequency (LF) power, and high-frequency (HF) power] and baroreflex sensitivity were increased in RGS2–/–. Atropine and atropine plus metoprolol markedly reduced RMSSD, LF, and HF. Our data suggest an interaction between RGS2 and the NO-cGMP pathway. The blunted L-NAME response in RGS2–/– during the day suggests impaired NO signaling. The MAP increases during the active phase in RGS2–/– mice may be related to central sympathetic activation and increased vascular adrenergic responsiveness.
nitric oxide-guanosine 3'-cyclic monophosphate pathway; regulator of G protein signaling 2-deficient mice; blood pressure; autonomic nervous system; spectral analysis; baroreflex
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