THE POWER SPECTRA RESPONSE OF STROKE VOLUME AND ARTERIAL BLOOD PRESSURE VARIABILITY SIGNALS TO AUTONOMIC NERVOUS SYSTEM MODULATION OF THE HEART

2009 ◽  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Stroke Volume ◽  
Arterial Blood Pressure ◽  
Blood Pressure Variability ◽  
Power Spectra ◽  
Autonomic Nervous ◽  
Arterial Blood

Paraventricular stimulation with glutamate elicits bradycardia and pituitary responses

1989 ◽  
Vol 256 (1) ◽  
pp. R112-R119 ◽  
Author(s):  
D. N. Darlington ◽  
M. Miyamoto ◽  
L. C. Keil ◽  
M. F. Dallman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Arterial Blood Pressure ◽  
Excitatory Neurotransmitter ◽  
Autonomic Nervous ◽  
Arterial Blood ◽  
Paraventricular Nuclei ◽  
Measured Activation

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.

Assessment of Autonomic Nervous System Via Dynamic Pupillometry in Different Circadian Arterial Blood Pressure Patterns

2018 ◽  
Vol 121 (8) ◽  
pp. e98-e99
Author(s):  
Sercan Okutucu ◽  
Mustafa Civelekler ◽  
Hakan Aksoy ◽  
Begum Yetis Sayin ◽  
Cengiz Sabanoglu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Arterial Blood Pressure ◽  
Autonomic Nervous ◽  
Arterial Blood ◽  
Blood Pressure Patterns

Abstract TMP97: Autonomic Nervous System Dysfunction Correlates With Increased Blood Pressure Variability After Acute Ischemic, But Not Hemorrhagic, Stroke

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Adam H de Havenon ◽  
Melissa Cortez ◽  
Cecilia Peterson ◽  
Fa Tuuhetaufa ◽  
Nils Petersen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Blood Pressure Variability ◽  
Hemorrhagic Stroke ◽  
Light Stimulus ◽  
Pupillary Response ◽  
Autonomic Nervous System Dysfunction ◽  
Autonomic Nervous ◽  
The Mean

Background: Elevated blood pressure variability (BPV) in the days after acute stroke onset is associated with worse outcome. However, the mechanism of increased BPV remains unknown, but may be due to dysfunction of the autonomic nervous system, which can be measured by pupil response to a light stimulus. Methods: This is a retrospective study of 109 patients in a neurocritical care unit: 45 with acute ischemic stroke (AIS), 44 with intracerebral hemorrhage (ICH), and 20 with subarachnoid hemorrhage (SAH). The primary outcome is BPV, measured as standard deviation of SBP (SD), using all blood pressures from admission to 72 hours later. The primary predictors are pupillary light reflexes (PLR) from the same period, measured with a bedside pupilometer, the NPi-200. We used linear regression to evaluate the association between PLRs and BPV, and adjusted for patient age and gender. Results: The mean (SD) age was 60.7 (16.4) and 58.7% were male. The mean (SD) number of blood pressure and PLR measurements were 30.0 (9.0) and 10.4 (7.3). We found that parasympathetically mediated PLR measures were associated with BPV in AIS patients (Table 1), but no consistent pattern emerged in ICH or SAH patients (all p>0.05). The relationships between BPV and PLR for AIS patients were linear in nature (Figure 1), and were consistent with parasympathetic hypofunction in patients with the greatest BPV. Conclusions: Elevated BPV is associated with parasympathetic hypofunction, as measured by pupillary response to light, after acute ischemic, but not hemorrhagic, stroke. Further research is needed to better understand this relationship as it may represent a therapeutic target for BPV reduction.

Role of angiotensin and vasopressin on blood pressure of ganglionic blocked dogs

1983 ◽  
Vol 244 (1) ◽  
pp. H115-H120 ◽  
Author(s):  
P. C. Houck ◽  
M. J. Fiksen-Olsen ◽  
S. L. Britton ◽  
J. C. Romero
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Vasopressin Antagonist ◽  
Ganglionic Blockade ◽  
Autonomic Nervous ◽  
Arterial Blood ◽  
Group 2 ◽  
Group 1

This study was designed to investigate the possible role of angiotensin and vasopressin in the maintenance of arterial blood pressure during acute blockade of the autonomic nervous system. Two groups of eight dogs each were anesthetized with pentobarbital sodium, and autonomic ganglia were blocked with hexamethonium (20 mg/kg). Thirty minutes later group 1 received the vasopressin antagonist 1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid),2-(O-methyl)tyrosine arginine vasopressin (10 micrograms/kg) followed after a 30-min interval by captopril (1 mg/kg). Group 2 received the same drugs, except the order of administration of vasopressin antagonist and captopril was reversed. Vasopressin antagonist during ganglionic blockade (group 2) produced a greater fall in blood pressure than did captopril during ganglionic blockade (group 1). These data indicate that vasopressin plays a greater pressor role than angiotensin in the acute response to ganglionic blockade. Additional studies were performed to determine if the autonomic nervous system alone can support the resting blood pressure in the anesthetized dog. Combined blockade of angiotensin and vasopressin without autonomic blockade produced a significant decrease in blood pressure, suggesting that the autonomic nervous system alone is not able to support the control blood pressure in the anesthetized dog.

Support of arterial blood pressure by major pressor systems in conscious dogs

1988 ◽  
Vol 255 (3) ◽  
pp. H483-H491 ◽  
Author(s):  
P. H. Brand ◽  
P. J. Metting ◽  
S. L. Britton
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Steady State ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Autonomic Function ◽  
Autonomic Ganglia ◽  
Arterial Blood

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.

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 ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Environmental Stress ◽  
G Protein ◽  
Arterial Blood Pressure ◽  
Stress Sensitivity ◽  
Pressure Regulation ◽  
Arterial Blood ◽  
Deficient Mice

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.

scholarly journals Blood pressure variability in relation to autonomic nervous system dysregulation: the X-CELLENT study

2011 ◽  
Vol 35 (4) ◽  
pp. 399-403 ◽  
Author(s):  
Yi Zhang ◽  
Davide Agnoletti ◽  
Jacques Blacher ◽  
Michel E Safar
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Blood Pressure Variability ◽  
Autonomic Nervous
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