Autonomic nervous system and blood pressure regulation in RGS2-deficient mice

2005 ◽  
Vol 288 (5) ◽  
pp. R1134-R1142 ◽  
Author(s):  
Volkmar Gross ◽  
Jens Tank ◽  
Michael Obst ◽  
Ralph Plehm ◽  
Kendall J. Blumer ◽  
...  

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.

1989 ◽  
Vol 256 (1) ◽  
pp. R112-R119 ◽  
Author(s):  
D. N. Darlington ◽  
M. Miyamoto ◽  
L. C. Keil ◽  
M. F. Dallman

The excitatory neurotransmitter, L-glutamate (0.5 M, pH 7.4), or the organic acid, acetate (0.5 M, pH 7.4), was microinjected (50 nl over 2 min) directly into the paraventricular nuclei (PVN) of pentobarbital sodium-anesthetized rats while arterial blood pressure and heart rate and plasma adrenocorticotropic hormone (ACTH), vasopressin, and oxytocin were measured. Activation of PVN neurons with L-glutamate led to increases in plasma ACTH, vasopressin, and oxytocin and a profound bradycardia (approximately 80 beats/min) with little change in arterial blood pressure. Microinjection of acetate had no effect on the above variables. The decrease in heart rate was shown to be dependent on the concentration of glutamate injected and the volume of injectate. The bradycardia was mediated through the autonomic nervous system because ganglionic blockade (pentolinium tartrate) eliminated the response; atropine and propranolol severely attenuated the bradycardia. The bradycardia was greatest when L-glutamate was microinjected into the caudal PVN. Injections into the rostral PVN or into nuclei surrounding the PVN led to small or nonsignificant decreases in heart rate. Focal electric stimulation (2-50 microA) of the PVN also led to decreases in heart rate and arterial blood pressure. These data suggest that activation of PVN neurons leads to the release of ACTH, vasopressin, and oxytocin from the pituitary and a bradycardia that is mediated by the autonomic nervous system.


1988 ◽  
Vol 255 (3) ◽  
pp. H483-H491 ◽  
Author(s):  
P. H. Brand ◽  
P. J. Metting ◽  
S. L. Britton

The roles of the autonomic nervous system, vasopressin, and angiotensin II in support of blood pressure were evaluated in seven conscious, resting dogs while hydrated or dehydrated. Mean arterial blood pressure (MAP) was monitored, and the dogs were given hexamethonium to block autonomic ganglia. Thirty minutes later, they were given captopril, and after another 30 min, a vasopressin V1 antagonist, d(CH2)5TyrMeAVP, was given. The order okf administration of captopril and d(CH2)5TyrMeAVP was alternated in different experiments. Hexamethonium had no effect on steady-state MAP in either hydrated or dehydrated dogs. In hydrated dogs, the average MAP was 100 mmHg; d(CH2)5TyrMeAVP decreased MAP by approximately 12 mmHg, and captopril decreased MAP by 24 mmHg. The magnitude of the effect of these two inhibitors was independent of the order of their administration. Dehydration doubled the effect of d(CH2)5TyrMeAVP on MAP but had no effect on the response to captopril. The results suggest that 1) autonomic function is not essential for maintenance of arterial blood pressure in resting dogs; 2) during autonomic ganglionic blockade, arterial blood pressure is supported by both angiotensin II and vasopressin; and 3) dehydration increases the role of vasopressin in control of blood pressure.


2018 ◽  
Vol 121 (8) ◽  
pp. e98-e99
Author(s):  
Sercan Okutucu ◽  
Mustafa Civelekler ◽  
Hakan Aksoy ◽  
Begum Yetis Sayin ◽  
Cengiz Sabanoglu ◽  
...  

2020 ◽  
Vol 129 (6) ◽  
pp. 1310-1323
Author(s):  
Jennifer L. Magnusson ◽  
Craig A. Emter ◽  
Kevin J. Cummings

The role of serotonin in arterial blood pressure (ABP) regulation across states of vigilance is unknown. We hypothesized that adult rats devoid of CNS serotonin (TPH2−/−) have low ABP in wakefulness and NREM sleep, when serotonin neurons are active. However, TPH2−/− rats experience higher ABP than TPH2+/+ rats in wakefulness and REM only, a phenotype present only in older males and not females. CNS serotonin may be critical for preventing high ABP in males with aging.


2006 ◽  
Vol 70 (6) ◽  
pp. 759-766 ◽  
Author(s):  
K. Yamagishi ◽  
T. Tanigawa ◽  
R. Cui ◽  
M. Tabata ◽  
A. Ikeda ◽  
...  

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