scholarly journals Chronic baroreflex activation restores spontaneous baroreflex control and variability of heart rate in obesity-induced hypertension

2013 ◽  
Vol 305 (7) ◽  
pp. H1080-H1088 ◽  
Author(s):  
Radu Iliescu ◽  
Ionut Tudorancea ◽  
Eric D. Irwin ◽  
Thomas E. Lohmeier
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Arterial Pressure ◽  
Cardiac Arrhythmias ◽  
High Fat Diet ◽  
Renal Denervation ◽  
Gradual Increase ◽  
High Fat ◽  
Baroreflex Control ◽  
Cardiovascular Dynamic

The sensitivity of baroreflex control of heart rate is depressed in subjects with obesity hypertension, which increases the risk for cardiac arrhythmias. The mechanisms are not fully known, and there are no therapies to improve this dysfunction. To determine the cardiovascular dynamic effects of progressive increases in body weight leading to obesity and hypertension in dogs fed a high-fat diet, 24-h continuous recordings of spontaneous fluctuations in blood pressure and heart rate were analyzed in the time and frequency domains. Furthermore, we investigated whether autonomic mechanisms stimulated by chronic baroreflex activation and renal denervation—current therapies in patients with resistant hypertension, who are commonly obese—restore cardiovascular dynamic control. Increases in body weight to ∼150% of control led to a gradual increase in mean arterial pressure to 17 ± 3 mmHg above control (100 ± 2 mmHg) after 4 wk on the high-fat diet. In contrast to the gradual increase in arterial pressure, tachycardia, attenuated chronotropic baroreflex responses, and reduced heart rate variability were manifest within 1–4 days on high-fat intake, reaching 130 ± 4 beats per minute (bpm) (control = 86 ± 3 bpm) and ∼45% and <20%, respectively, of control levels. Subsequently, both baroreflex activation and renal denervation abolished the hypertension. However, only baroreflex activation effectively attenuated the tachycardia and restored cardiac baroreflex sensitivity and heart rate variability. These findings suggest that baroreflex activation therapy may reduce the risk factors for cardiac arrhythmias as well as lower arterial pressure.

Stimulation of NPY Y2 receptors by PYY3-36 reveals divergent cardiovascular effects of endogenous NPY in rats on different dietary regimens

2004 ◽  
Vol 286 (1) ◽  
pp. R138-R142 ◽  
Author(s):  
Ulrich Nordheim ◽  
Karl G. Hofbauer
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
High Fat Diet ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Chow Diet ◽  
High Fat ◽  
Standard Chow Diet ◽  
Ad Libitum

In the present experiments the gut hormone peptide YY3-36 (PYY3-36), which inhibits neuropeptide Y (NPY) release, was used as a tool to study the cardiovascular effects of endogenous NPY under different dietary regimens in rats instrumented with a telemetry transmitter. In a first experiment, rats were placed on a standard chow diet ad libitum and in a second experiment on a high-fat diet ad libitum. After 6 wk, PYY3-36 (300 μg/kg) or vehicle was injected intraperitoneally. In a third experiment, PYY3-36 or vehicle was administered after 14 days of 50% restriction of a standard chow diet. In food-restricted rats, PYY3-36 increased mean arterial pressure (7 ± 1 mmHg, mean ± SE, P < 0.001 vs. saline, 1-way repeated-measures ANOVA with Bonferroni t-test) and heart rate (22 ± 4 beats/min, P < 0.001) during 3 h after administration. Conversely, PYY3-36 did not influence mean arterial pressure (0 ± 1 mmHg) and heart rate (-8 ± 5 beats/min) significantly in rats on a high-fat diet. Rats fed standard chow diet ad libitum showed an intermediate response (mean arterial pressure 4 ± 1 mmHg, P < 0.05, and heart rate 5 ± 2 beats/min, not significant). Thus, in our studies, divergent cardiovascular responses to PYY3-36 were observed in rats on different dietary regimens. These findings suggest that the cardiovascular effects of PYY3-36 depend on the hypothalamic NPY release, which is increased after chronic food restriction and decreased during a high-fat diet.

Abstract 20189: Renal Denervation With Neuron Targeted Nanoparticles Attenuates the Hypertension Associated With Obesity

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Lilei Yu ◽  
XiaoYa Zhou ◽  
Songyun Wang ◽  
Zhuo Wang ◽  
Bing Huang ◽  
...  
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Tetanus Toxin ◽  
High Fat Diet ◽  
Renal Denervation ◽  
Control Period ◽  
Nerve Fibers ◽  
Control Group ◽  
High Fat ◽  
Renal Sympathetic

Introduction: Obesity is associated with hypertension and increased renal sympathetic nervous activity, Our recent study indicated that autonomic denervation could be induced by nanoparticles.In addition, non-toxic fragment of tetanus toxin, known as tetanus toxin C fragment(TTC), which demonstrates extremely high affinity binding to the surfaces of neurons. Hypothesis: This study was to test the hypothesis that renal denervation with TTC-conjugated nanoparticles could attenuate hypertension associated with obesity . Methods: TTC-conjugated nanoparticles and neurotoxic agent (N-isopropylacrylamide monomer) were synthesized. We determined the hemodynamic responses to a high-fat diet in control (n = 6) and renal-denervated by nanoparticles (n = 8) chronically instrumented dogs. After a control period of 7 days, dogs were placed on a high-fat diet for 5 weeks. a modified balloon catheter will be advanced in the target renal artery segment to allow nanoparticles permeating into vascular wall, after that the moving of nanoparticles will be guided by outside magnetic filed towards renal sympathetic nerve.Blood pressure(BP),heart rate variability (HRV),serum norepinephrine (NE) were measured. Pathological examinations were performed on all retrieved samples. Results: In response to a high-fat diet, body weight increased from 17.6 ± 2.4 to 24.8 ± 1.8 kg in the control group. Heart rate increased from 92 ± 6 to 118 ± 10 beats per minute in the control group. BP increased significantly from 105 ± 5 to 139 ± 4 mm Hg in the control group. In contrast, 5 weeks of a high-fat diet in the renal denervation group did not significantly increase body weight(which went from 18.3 ± 2.5 to 19 ± 2.1 mm Hg), Heart rate (which went from 87 ± 3 to 89 ± 6 mm Hg) and BP (which went from 107 ± 3 to 109 ± 6 mm Hg). sympathetic indices of HRV, serum NE, renal sympathetic activity and the expression of c-fos protein in renal sympathetic nerve was significantly lower in the renal denervation group. A histological examination revealed the disruption of nerve fibers, necrosis of Schwann cells and neurons, and apparent denervation in denervation group. Conclusions: Our results indicate that Renal denervation by TTC-conjugated nanoparticles could attenuate hypertension associated with obesity.

Baroreflex sensitivity in the canine model of obesity-induced hypertension

1990 ◽  
Vol 259 (5) ◽  
pp. R981-R985 ◽  
Author(s):  
K. E. Wehberg ◽  
D. B. West ◽  
C. Kieswetter ◽  
J. P. Granger
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
High Fat Diet ◽  
Baroreflex Sensitivity ◽  
Canine Model ◽  
High Fat ◽  
Induced Hypertension

Studies have demonstrated abnormalities in baroreflex function in various models of hypertension. The purpose of this study was to examine baroreflex sensitivity in the canine model of obesity-induced hypertension. Baroreflex sensitivity was determined by the relative changes in heart rate (HR) in response to changes in mean arterial pressure (MAP) induced by sodium nitroprusside (Nitro) and phenylephrine (Pe). Studies were performed in conscious lean dogs (n = 10) and obese dogs fed a high-fat diet for 6 wk (n = 8). Body weight averaged 18.1 +/- 0.3 kg in the lean dogs and 26.5 +/- 0.5 kg in the obese dogs. Associated with the 46% increase in body weight in the obese dog group were significant increases in MAP (120.7 +/- 3.0 vs. 102.8 +/- 1.5 mmHg) and HR (132.7 +/- 8.5 vs. 96.4 +/- 3.3 beats/min). Administration of Nitro (0.5, 1.0, 5.0 micrograms.kg-1.min-1) resulted in comparable reductions in MAP in the lean and obese dogs. The reflex increases in HR were significantly greater in the obese animals only with a dose of 5.0 micrograms.kg-1.min-1 of Nitro (55.5 +/- 7.7 vs. 32.0 +/- 7.5 beats/min). Administration of Pe (0.5, 1.0, 5.0 micrograms.kg-1.min-1) resulted in significantly greater increases in MAP in the obese dogs (17.8 +/- 4.6 vs. 4.9 +/- 2.6, 37.1 +/- 4.4 vs. 19.6 +/- 2.7, and 72.7 +/- 7.5 vs. 51.5 +/- 7.1 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Acute overconsumption of a high‐fat diet alters heart rate variability

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Matt Owings ◽  
Ana K Wilson ◽  
Kimberly J Winterrowd ◽  
Joan F Carroll
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
High Fat Diet ◽  
High Fat

Electrical stimulation of the carotid sinus lowers arterial pressure and improves heart rate variability in l-NAME hypertensive conscious rats

2020 ◽  
Vol 43 (10) ◽  
pp. 1057-1067 ◽  
Author(s):  
Gean Domingos-Souza ◽  
Fernanda Machado Santos-Almeida ◽  
César Arruda Meschiari ◽  
Nathanne S. Ferreira ◽  
Camila A. Pereira ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Conscious Rats ◽  
Stimulation Of

High-fat diet is associated with blunted splanchnic sympathoinhibitory responses to gastric leptin and cholecystokinin: implications for circulatory control

2011 ◽  
Vol 300 (3) ◽  
pp. H961-H967 ◽  
Author(s):  
Jackie M. Y. How ◽  
Barbara C. Fam ◽  
Anthony J. M. Verberne ◽  
Daniela M. Sartor
Keyword(s):  
Arterial Pressure ◽  
High Fat Diet ◽  
Cardiovascular Effects ◽  
Vagal Afferents ◽  
Sprague Dawley ◽  
High Fat ◽  
Lower Plasma ◽  
Lower Tertile ◽  
Circulatory Control ◽  
Plasma Leptin

Gastric leptin and cholecystokinin (CCK) act on vagal afferents to induce cardiovascular effects and reflex inhibition of splanchnic sympathetic nerve discharge (SSND) and may act cooperatively in these responses. We sought to determine whether these effects are altered in animals that developed obesity in response to a medium high-fat diet (MHFD). Male Sprague-Dawley rats were placed on a low-fat diet (LFD; n = 8) or a MHFD ( n = 24) for 13 wk, after which the animals were anesthetized and artificially ventilated. Arterial pressure was monitored and blood was collected for the determination of plasma leptin and CCK. SSND responses to leptin (15 μg/kg) and CCK (2 μg/kg) administered close to the coeliac artery were evaluated. Collectively, MHFD animals had significantly higher plasma leptin but lower plasma CCK levels than LFD rats ( P < 0.05), and this corresponded to attenuated or reversed SSND responses to CCK (LFD, −21 ± 2%; and MHFD, −12 ± 2%; P < 0.05) and leptin (LFD, −6 ± 2%; and MHFD, 4 ± 1%; P < 0.001). Alternatively, animals on the MHFD were stratified into obesity-prone (OP; n = 8) or obesity-resistant (OR; n = 8) groups according to their weight gain falling within the upper or lower tertile, respectively. OP rats had significantly higher resting arterial pressure, adiposity, and plasma leptin but lower plasma CCK compared with LFD rats ( P < 0.05). The SSND responses to CCK or leptin were not significantly different between OP and OR animals. These results demonstrate that a high-fat diet is associated with blunted splanchnic sympathoinhibitory responses to gastric leptin and CCK and may impact on sympathetic vasomotor mechanisms involved in circulatory control.

Abstract 477: Chronic Baroreflex Activation Improves Baroreflex Control of Heart Rate In Obesity

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Radu Iliescu ◽  
Ionut Tudorancea ◽  
Eric Irwin ◽  
Thomas Lohmeier
Keyword(s):  
Heart Rate ◽  
Pulse Interval ◽  
Vagal Activity ◽  
Fat Intake ◽  
High Fat ◽  
Baroreflex Control ◽  
Systolic Blood Pressure Variability ◽  
Body Weight Increase ◽  
Obesity Hypertension ◽  
Fat Feeding

Impaired baroreflex control of heart rate (BRS) and attendant risk for cardiac arrhythmias are associated with sympathetically-mediated obesity hypertension. Since both global and renal-specific sympathoinhibition have sustained antihypertensive effects in obesity, we compared BRS in obese dogs subjected to 7 days of electrical baroreflex activation (BA) and, after recovery (REC), to bilateral surgical renal denervation (RDX). After control (C) measurements and 4 weeks of high fat diet, fat intake was reduced (RF) to maintain a body weight increase of ∼ 50%, which led to an increase in mean arterial pressure (MAP) from 100±2 to 117±3 mmHg and heart rate (HR) from 86±3 to 130±4 bpm. Obesity hypertension was associated with decreased sensitivity of 24h spontaneous BRS (determined by the sequence technique from daily beat-to-beat time series) and pulse interval (PI) variability (24h SD). While both BA and RDX abolished hypertension, only BA diminished tachycardia and normalized BRS, consequently improving HR variability. Short-term systolic blood pressure variability (5 min SD) also decreased with high fat feeding and was restored to control upon reduction of fat intake (RF) during established obesity hypertension, suggesting a vasoplegic effect of fat. These data suggest that in addition to the antihypertensive effects of sympathoinhibition, BA corrects cardiac baroreflex dysfunction in obesity hypertension, presumably by enhancing cardiac vagal activity. This in turn markedly improves depressed HR variability, a known risk factor for cardiac arrhythmic events.

Compensatory recovery of parasympathetic control of heart rate after unilateral vagotomy in rabbits

1992 ◽  
Vol 262 (4) ◽  
pp. H1122-H1127 ◽  
Author(s):  
D. D. Lund ◽  
G. A. Davey ◽  
A. R. Subieta ◽  
B. J. Pardini
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Nerve Stimulation ◽  
Vagal Stimulation ◽  
Acetylcholinesterase Inhibition ◽  
Baroreflex Control ◽  
Recovery Mechanism ◽  
Vagal Innervation ◽  
Increased Sensitivity ◽  
Parasympathetic Control

Compensatory recovery by the intact vagal innervation after unilateral vagotomy was investigated by measuring parasympathetic-mediated control of heart rate in beta-adrenergic-blocked rabbits. Direct contralateral vagal nerve stimulation produced greater bradycardia in anesthetized rabbits with chronic vagotomy compared with acutely vagotomized controls. Vagal stimulation during acetylcholinesterase inhibition by physostigmine and direct neuroeffector stimulation by methacholine indicated that a change in metabolism of the neurotransmitter or an increased sensitivity of the tissue to acetylcholine were not responsible for augmentation of vagal responses. Baroreflex control of heart rate in response to an increase in arterial pressure was also tested in urethan-anesthetized rabbits. There was a significant reduction in the prolongation of the R-R interval during baroreflex activation acutely after midcervical vagotomy. These values were subsequently above control levels in rabbits 28 days after vagotomy. In conscious rabbits, the decrease in baroreflex control of heart rate progressively recovered to control levels within 6 days. These results suggest that the recovery mechanism after unilateral vagotomy may be related to peripheral and central compensatory changes in the intact contralateral vagus nerve.

scholarly journals Use of Ethylmethylhydroxypyridine in Patients Presenting with Myocardial Infarction: Antiischemic, Antidepressant, Anxiolytic Effects

2016 ◽  
pp. 67-74
Author(s):  
Maryna Dolzhenko ◽  
Olena Popovich ◽  
Oksana Shershnyova ◽  
Oleksandr Nudchenko ◽  
Kardo Faradzh ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Mental State ◽  
Cardiac Arrhythmias ◽  
Average Score ◽  
Control Group ◽  
Basic Therapy ◽  
Coronary Syndrome ◽  
St Segment

The objective: to evaluate the efficiency of ethylmethylhydroxypyridine (Mexiprim, STADA Arzneimittel AG, Germany) in patients presenting with myocardial infarction at hospital and outpatient stage. Patients and methods. The study included 59 patients with coronary artery disease, acute coronary syndrome with ST1segment elevation in the first day of admission to the ICU, AH, 3-stage, 2 degrees, HF. To all patients basic therapy according to current ESH/ESC guidelines was prescribed. To 39 patients additionally intravenous infusion of 200 mg of mexiprim o.d. for 10 days, followed by 125 mg per os three times a day for next 60 days was administered. Another 20 patients presented control group and received only basic therapy. The study design included: 24-hour Holter monitoring to estimate the dynamics of changes in the ST segment, cardiac arrhythmias and heart rate variability, evaluation by the scale of Beck, Hamilton scale for the assessment of anxiety (HARS) and depression (HDRS), the common blood and urine tests, biochemical blood analysis, evaluation of therapeutic tolerability conducted before treatment and 60 days after treatment. Surveys on a scale SAN, assessment of cognitive impairment on the MMSE scale were performed on the 60th day of treatment. Efficiency criteria were: a 50% reduction of cardiac arrhythmias, a decrease in ischemia, a decrease by 50% or more from baseline average score by HARS, HDRS scales, dynamics of the mental state questionnaire and less than 9 points on a scale of depression, reducing in SAN scale score. Results. In pаtients of mexiprim group significant reduction of depression scores by 62% were observed. According to the dynamics of the mental state questionnaire patients of mexiprim group reported feeling better, that is, reduction of score by 45% . According to the Hamilton scale for the assessment of anxiety (HARS), in particular mental anxiety – decrease in the total score of 65%, somatic anxiety – by 35.5%, and a total of 50% were revealed. In the group of patients receiving additionally intravenous Mexiprim for 10 days significantly reduced the number of single and group PACs, as well as single and multiple PVCs, not only in comparison with these parameters before the treatment, but also in comparison with the control group. In patients treated with Mexiprim no evidence of residual ischaemia were noted, but in the control group statistically significant segment depression ST remained. Heart rate variability was not significantly changed in the control group, but increased in patients who received Mexiprim. Conclusion. Use of Mexiprim in patients with myocardial infarction reduces ST segment depression, amount of ventricular and supraventricular arrhythmias, improved heart rate variability, and the state of anxiety and depression.

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