scholarly journals Regulation of blood pressure by the central nucleus of the amygdala in dynamically changing appetitive and aversive classical conditioning tasks in rats

2021 ◽  
Author(s):  
Ko Yamanaka ◽  
Hidefumi Waki
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Classical Conditioning ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Central Nucleus ◽  
Conditioned Stimuli ◽  
Neuronal Mechanisms ◽  
Aversive Classical Conditioning

Abstract In an environment of dynamically changing conditions, humans and animals can determine whether a current situation is favorable to them and accordingly select actions. Autonomic cardiovascular tuning is as important as motor control for this function. However, neuronal mechanisms underlying the dynamic adjustments of autonomic cardiovascular responses remain unclear. In this study, we hypothesized that the amygdala plays a role in autonomic cardiovascular tuning in a dynamically changing situation. We recorded the blood pressures and heart rates of head-restrained rats during appetitive and aversive classical conditioning tasks. Rats learned varying associations between conditioned stimuli and unconditioned stimuli in appetitive, neutral, and aversive blocks. Blood pressure and heart rate in the appetitive block gradually increased in response to reward-predicting cue, preceded by a vigorously increased response to the actual reward. The predictive response was significantly higher than the responses in the neutral and aversive condition blocks. Blood pressure and heart rate responses to the air puff-predicting cue in the aversive block were significantly lower than that of the responses in the neutral block. The conditioned blood pressure response rapidly changed through condition switching. Furthermore, bilateral pharmacological inactivation of the central nucleus of the amygdala has significantly decreased reward-predictive pressor responses in the latter phase, but not in the initial phase of block change. These results suggest that blood pressure is adaptively tuned by positive and negative conditioned stimuli and that the central nucleus of the amygdala likely assists in maintaining pressor response in dynamically changing situations.

scholarly journals Maintenance of Blood Pressure in Emotional Context-based Autonomic Switching by the Central Nucleus of the Amygdala in Rats

2020 ◽  
Author(s):  
Ko Yamanaka ◽  
Hidefumi Waki
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Central Nucleus ◽  
Emotional Context ◽  
Neuronal Mechanisms ◽  
Pressor Responses ◽  
Pharmacological Blockade ◽  
Aversive Classical Conditioning

Abstract Proper autonomic control is necessary in making appropriate decisions and actions, but neuronal mechanisms for this function are yet to be determined. Here we show that the amygdala plays a role in autonomic cardiovascular tuning in a dynamically changing environment. We recorded blood pressure and heart rate of head-restrained rats during appetitive and aversive classical conditioning tasks. Rats learned varying associations between conditioned stimuli and unconditioned stimuli in three types of contexts: appetitive, neutral, and aversive blocks. Blood pressure and heart rate in the appetitive block gradually increased after reward-predicting cues, followed by a vigorously increased response to the actual reward. The predictive response was found to be significantly higher than the responses in the neutral and aversive blocks. Blood pressure and heart rate responses to the air puff-predicting cue in the aversive block were significantly lower than that of the responses in the neutral block. Pharmacological blockade of the amygdala has significantly decreased reward-predictive pressor responses in the latter phase, but not in the initial phase of context change. Cardiovascular responses are thus adaptively tuned by positive and negative emotional stimuli, and the central nucleus of the amygdala likely assists in maintaining pressor response tuning based on emotional context.

Blunted blood pressure response to exercise and isolated muscle metaboreflex activation in patients with cirrhosis

2020 ◽  
Author(s):  
Pedro Augusto Carvalho Mira ◽  
Maria Fernanda Almeida Falci ◽  
Janaína Becari Moreira ◽  
Rosa Virginia Diaz Guerrero ◽  
Tarsila Campanha da Rocha Ribeiro ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Pressure Response ◽  
Isometric Handgrip ◽  
Muscle Metaboreflex ◽  
Cirrhotic Patients ◽  
Response To Exercise

We sought to test the hypothesis that the cardiovascular responses to isolated muscle metaboreflex activation would be blunted in patients with cirrhosis. Eleven patients with cirrhosis and 15 healthy controls were evaluated. Blood pressure (BP, oscillometric method), contralateral forearm blood flow (FBF, venous occlusion plethysmography) and heart rate (HR, electrocardiogram) were measured during baseline, isometric handgrip at 30% of maximal voluntary contraction followed by post-exercise ischemia (PEI). Forearm vascular conductance (FVC) was calculated as follows: (FBF/mean BP) x 100. Changes in HR during handgrip were similar between groups, but tended to be different during PEI (controls: ∆0.5 ± 1.1 bpm vs. cirrhotic patients: ∆3.6 ± 1.0 bpm, P = 0.057). Mean BP response to handgrip (controls: ∆20.9 ± 2.7 mmHg vs. cirrhotic patients: ∆10.6 ± 1.5 mmHg, P = 0.006) and PEI was attenuated in cirrhotic patients (controls: ∆16.1 ± 1.9 mmHg vs. cirrhotic patients: ∆7.2 ± 1.4 mmHg, P = 0.001). In contrast, FBF and FVC increased during handgrip and decreased during PEI similarly between groups. These results indicate that an abnormal muscle metaboreflex activation explained, at least partially, the blunted pressor response to exercise exhibited by cirrhotic patients. Novelty bullets: • Patients with cirrhosis present abnormal muscle metaboreflex activation • Blood pressure response was blunted, but forearm vascular response was preserved • Heart rate response was slightly elevated

Yohimbine-precipitated clonidine withdrawal: An experimental model of the antihypertensive drug withdrawal syndrome

1992 ◽  
Vol 70 (6) ◽  
pp. 853-858 ◽  
Author(s):  
Donald H. Penning ◽  
Khem Jhamandas
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Intravenous Injection ◽  
Withdrawal Syndrome ◽  
Adrenergic Receptor ◽  
Blood Pressure Response ◽  
Late Phase ◽  
Cardiovascular Responses ◽  
Atropine Sulfate ◽  
Clonidine Withdrawal

In this study, a model of the clonidine withdrawal syndrome in normotensive rats was used to investigate the mechanisms and sites of the cardiovascular responses associated with this withdrawal. Clonidine (400 μg∙kg−1∙day−1), an α2-adrenergic receptor agonist, was administered to rats via indwelling osmotic minipumps for 7 days. Withdrawal was precipitated by an intravenous injection of the α2-adrenergic receptor antagonist yohimbine under α-chloralose anaesthesia, and the blood pressure and heart rate responses were recorded. Yohimbine (0.25, 0.50, and 1.0 mg/kg i.v.) in clonidine-treated rats provoked an immediate rise in blood pressure and heart rate. Similar injections in saline-treated rats produced slight hypotension and modestly increased the heart rate. Intracerebroventricular (i.c.v.) yohimbine injection (30 or 120 μg/kg in 10 μL volume) failed to elicit signs of withdrawal in clonidine-treated animals, but a subsequent intravenous injection of yohimbine (0.5 mg/kg) provoked brisk signs of withdrawal. Hexamethonium (2 mg/kg) pretreatment did not abolish the increase in the heart rate, but it delayed the blood pressure increase. Pretreatment with atropine sulfate (1 mg/kg) did not block the yohimbine-induced increase in heart rate or blood pressure. This study demonstrates that yohimbine can effectively produce cardiovascular signs of withdrawal in rats chronically exposed to clonidine. The lack of i.c.v. yohimbine suggests that the antagonist-precipitated withdrawal may not have a central origin. The failure of atropine to attenuate the blood pressure and heart rate responses, and the failure of hexamethonium to block the heart rate response and the late phase of blood pressure response, suggest that central cholinergic hyperactivity is not substantially involved in the yohimbine-precipitated clonidine withdrawal. It is suggested that under the conditions of clonidine exposure used here, the yohimbine-precipitated response may arise from increased activity of peripheral sympathetic mechanisms.Key words: yohimbine, clonidine withdrawal syndrome.

Cardiovascular consequences of microinjection of vasopressin and angiotensin II in the area postrema

1993 ◽  
Vol 265 (3) ◽  
pp. R625-R631 ◽  
Author(s):  
V. L. Lowes ◽  
L. E. McLean ◽  
N. W. Kasting ◽  
A. V. Ferguson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Area Postrema ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Systemic Administration ◽  
Pressure Response ◽  
Arterial Blood ◽  
At1 Antagonist

Microinjection of angiotensin II (ANG II) into the area postrema (AP) of urethan-anesthetized male Sprague-Dawley rats elicited statistically significant increases in mean arterial blood pressure at doses ranging from 10 pg to 500 ng (10 pg, mean +/- SE, 10.8 +/- 1.1 mmHg, P < 0.001; 250 ng, 15.2 +/- 2.6 mmHg, P < 0.001). Heart rate was also significantly increased at doses > 10 pg, although these increases were not dose dependent. Systemic administration of losartan (Dup-753), an AT1 antagonist, was able to significantly reduce the pressor response to 250 ng ANG (post-losartan: 81.9 +/- 9.5% reduction in blood pressure response, P < 0.0001), whereas PD123319, an AT2 antagonist, was without significant effect (P > 0.1). Microinjection of vasopressin (VP) (10 pg-500 ng) into the AP also resulted in statistically significant increases in blood pressure at doses ranging from 10 to 100 pg (10 pg, 7.0 +/- 1.5 mmHg, P < 0.05) and 100-500 ng (250 ng, 12.2 +/- 1.8 mmHg, P < 0.0001). Small but significant changes in heart rate were observed only at 100 pg and 100 ng. Systemic administration of a V1 antagonist significantly attenuated the increases in blood pressure in response to 50, 100, and 250 ng VP (250 ng, post-V1 antagonist: 66.4 +/- 8.6% reduction in blood pressure response, P < 0.001), whereas [desamino,D-Arg8]vasopressin (DDAVP), a V2 agonist, had a depressor effect when microinjected directly into the AP (250 ng, -9.9 +/- 1.6 mmHg, P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Hormonal, metabolic, and cardiovascular responses to static exercise in humans: influence of epidural anesthesia

1991 ◽  
Vol 261 (2) ◽  
pp. E214-E220 ◽  
Author(s):  
M. Kjaer ◽  
N. H. Secher ◽  
F. W. Bach ◽  
H. Galbo ◽  
D. R. Reeves ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Epidural Anesthesia ◽  
Pressor Response ◽  
Plasma Concentrations ◽  
Cardiovascular Responses ◽  
Knee Extension ◽  
Voluntary Contraction ◽  
Static Exercise ◽  
Exercise In Humans

To determine the role of reflex neural mechanisms for hormonal, metabolic, heart rate (HR), and blood pressure (MABP) changes during static exercise, seven health young males performed 10-min periods of two-legged static knee extension both during control and during epidural anesthesia. Comparisons were made at identical absolute (29 Nm) and relative [15% maximal voluntary contraction (MVC)] force. Afferent nerve blockade was verified by hypesthesia below T10-T12 and attenuated postexercise ischemic pressor response. Leg strength was reduced to 67 +/- 5% of control. At same relative force, increases in MABP and HR occurred more rapidly without than with epidural anesthesia (P less than 0.05). This difference was diminished during identical absolute force. Changes in plasma concentrations of catecholamines followed the pattern of HR and MABP responses, with differences between epidural and control experiments being most pronounced early in the work period. Plasma beta-endorphin was elevated only after control exercise. No response at 15% MVC was found for growth hormone, adrenocorticotropic hormone, insulin, glucagon, cortisol, glycerol, free fatty acids, or glucose (P greater than 0.05). In conclusion, during static exercise with large muscle groups and moderate relative force, modest changes in plasma hormones and metabolites take place. Furthermore, afferent nervous feedback from contracting muscles is important in regulation of blood pressure, heart rate, and catecholamine responses during static exercise in humans.

Effects of angiotensin II on autonomic components of nasopharyngeal stimulation in male conscious rabbits

2005 ◽  
Vol 98 (5) ◽  
pp. 1607-1611 ◽  
Author(s):  
Tarek M. Mousa ◽  
Lie Gao ◽  
Kurtis G. Cornish ◽  
Irving H. Zucker
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Cigarette Smoke ◽  
Pressor Response ◽  
Sympathetic Neurons ◽  
Cardiovascular Responses ◽  
Ang Ii ◽  
Before And After ◽  
Conscious Rabbits

Angiotensin II (ANG II) is known to activate central sympathetic neurons. In this study we determined the effects of ANG II on the autonomic components of the cardiovascular responses to stimulation of nasopharyngeal receptors with cigarette smoke. Experiments were carried out in conscious New Zealand White rabbits instrumented to record arterial pressure and heart rate. Rabbits were exposed to 50 ml of cigarette smoke before and after subcutaneous osmotic minipump delivery of ANG II at a dose of 50 ng·kg−1·min−1 for 1 wk in one group and intracerebroventricular (icv) infusion at a dose of 100 pmol/min for 1 h in a second group. The responses were compared before and after heart rate was controlled by pacing. Autonomic components were evaluated by intravenous administration of atropine methyl bromide (0.2 mg/kg) and prazosin (0.5 mg/kg). ANG II given either systemically or icv significantly blunted the pressor response to smoke ( P < 0.05) when the bradycardic response was prevented. This blunted response was not due to an absolute increase in baseline blood pressure after ANG II infusion (71.64 ± 11.6 vs. 92.1 ± 19.8 mmHg; P < 0.05) because normalization of blood pressure with sodium nitroprusside to pre-ANG II levels also resulted in a significantly blunted pressor response to smoke. The effect of smoke was α1-adrenergic receptor-mediated because it was essentially abolished by prazosin in both the pre- and the post-ANG II states ( P < 0.05). These results suggest that elevations in central ANG II reduce the sympathetic response to smoke in conscious rabbits. This effect may be due to an augmentation of baseline sympathetic outflow and a reduction in reflex sensitivity similar to the effect of ANG II on baroreflex function.

Resistance-training experience and the pressor response during resistance exercise

1987 ◽  
Vol 63 (1) ◽  
pp. 116-120 ◽  
Author(s):  
S. J. Fleck ◽  
L. S. Dean
Keyword(s):  
Heart Rate ◽  
Resistance Training ◽  
Heart Rate Response ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Dynamic Resistance ◽  
Peak Heart Rate ◽  
Training Experience ◽  
Arterial Blood

The purpose of this study was to examine the effects previous resistance-training experience has on the cardiovascular responses to resistance-training exercises. To investigate this, the intra-arterial blood pressure response of four body builders (BB), six novice weight-trained individuals (NT), and six sedentary controls (SC) were monitored during performance of one-arm overhead presses and one-leg knee extensions. One repetition at the maximal weight possible (1 RM) and sets to voluntary fatigue at 90, 80, 70, and 50% of 1 RM were performed. Across groups, the BB demonstrated a significantly (P less than 0.05) lower peak and a lesser magnitude of response (changes from rest to peak) for systolic and diastolic blood pressures than the the NT and SC groups during both exercises. The BB also demonstrated significantly lower values across groups for peak heart rate and magnitude of heart rate response during arm presses. During knee extensions across groups, peak heart rate but not magnitude of the heart rate response was significantly lower in the BB. The results indicate that previous weight-training experience reduces the pressor response to dynamic resistance exercises.

Cardiovascular Responses to Muscle Stretching: A Systematic Review and Meta-analysis

2021 ◽  
Author(s):  
Ewan Thomas ◽  
Marianna Bellafiore ◽  
Ambra Gentile ◽  
Antonio Paoli ◽  
Antonio Palma ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular System ◽  
Vascular Function ◽  
Meta Analysis ◽  
Random Effect ◽  
Cardiovascular Responses ◽  
Qualitative Description ◽  
Cross Sectional ◽  
Quantitative Synthesis

AbstractThe aim of this study will be to review the current body of literature to understand the effects of stretching on the responses of the cardiovascular system. A literature search was performed using the following databases: Scopus, NLM Pubmed and ScienceDirect. Studies regarding the effects of stretching on responses of the cardiovascular system were investigated. Outcomes regarded heart rate(HR), blood pressure, pulse wave velocity (PWV of which baPWV for brachial-ankle and cfPWV for carotid-femoral waveforms), heart rate variability and endothelial vascular function. Subsequently, the effects of each outcome were quantitatively synthetized using meta-analytic synthesis with random-effect models. A total of 16 studies were considered eligible and included in the quantitative synthesis. Groups were also stratified according to cross-sectional or longitudinal stretching interventions. Quality assessment through the NHLBI tools observed a “fair-to-good” quality of the studies. The meta-analytic synthesis showed a significant effect of d=0.38 concerning HR, d=2.04 regarding baPWV and d=0.46 for cfPWV. Stretching significantly reduces arterial stiffness and HR. The qualitative description of the studies was also supported by the meta-analytic synthesis. No adverse effects were reported, after stretching, in patients affected by cardiovascular disease on blood pressure. There is a lack of studies regarding vascular adaptations to stretching.

Variability of the haemodynamic responses to laboratory tests employed in assessment of neural cardiovascular regulation in man

1985 ◽  
Vol 69 (5) ◽  
pp. 533-540 ◽  
Author(s):  
Gianfranco Parati ◽  
Guido Pomidossi ◽  
Agustin Ramirez ◽  
Bruno Cesana ◽  
Giuseppe Mancia
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Test Performance ◽  
Blood Pressure Response ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Cardiovascular Regulation ◽  
Pressor Test ◽  
Carotid Baroreceptor ◽  
Baroreceptor Stimulation

1. In man evaluation of neural cardiovascular regulation makes use of a variety of tests which address the excitatory and reflex inhibitory neural influences that control circulation. Because interpretation of these tests is largely based on the magnitude of the elicited haemodynamic responses, their reproducibility in any given subject is critical. 2. In 39 subjects with continuous blood pressure (intra-arterial catheter) and heart rate monitoring we measured (i) the blood pressure and heart rate rises during hand-grip and cold-pressor test, (ii) the heart rate changes occurring during baroreceptor stimulation and deactivation by injection of phenylephrine and trinitroglycerine, and (iii) the heart rate and blood pressure changes occurring with alteration in carotid baroreceptor activity by a neck chamber. Each test was carefully standardized and performed at 30 min intervals for a total of six times in each subject. 3. The results showed that the responses to any test were clearly different from one another and that this occurred in all subjects studied. For the group as a whole the average response variability (coefficient of variation) ranged from 10.2% for the blood pressure response to carotid baroreceptor stimulation to 44.2% for the heart rate response to cold-pressor test. The variability of the responses was not related to basal blood pressure or heart rate, nor to the temporal sequence of the test performance. 4. Thus tests employed for studying neural cardiovascular control in man produce responses whose reproducibility is limited. This phenomenon may make it more difficult to define the response magnitude typical of each subject, as well as its comparison in different conditions and diseases.

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