Faculty Opinions recommendation of Chronic baroreflex activation restores spontaneous baroreflex control and variability of heart rate in obesity-induced hypertension.

2013 ◽  
Author(s):  
Michael Andresen
Keyword(s):  
Heart Rate ◽  
Baroreflex Control ◽  
Induced Hypertension ◽  
Spontaneous Baroreflex

Spontaneous baroreflex control of heart rate versus cardiac output: altered coupling in heart failure

2008 ◽  
Vol 294 (3) ◽  
pp. H1304-H1309 ◽  
Author(s):  
Javier A. Sala-Mercado ◽  
Masashi Ichinose ◽  
Robert L. Hammond ◽  
Matthew Coutsos ◽  
Tomoko Ichinose ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Baroreflex Control ◽  
Ventricular Systolic Pressure ◽  
Linear Relationships ◽  
Before And After ◽  
Spontaneous Baroreflex

Dynamic cardiac baroreflex responses are frequently investigated by analyzing the spontaneous reciprocal changes in arterial pressure and heart rate (HR). However, whether the spontaneous baroreflex-induced changes in HR translate into changes in cardiac output (CO) is unknown. In addition, this linkage between changes in HR and changes in CO may be different in subjects with heart failure (HF). We examined these questions using conscious dogs before and after pacing-induced HF. Spontaneous baroreflex sensitivity in the control of HR and CO was evaluated as the slopes of the linear relationships between HR or CO and left ventricular systolic pressure (LVSP) during spontaneous sequences of greater or equal to three consecutive beats when HR or CO changed inversely versus pressure. Furthermore, the translation of baroreflex HR responses into CO responses (HR-CO translation) was examined by computing the overlap between HR and CO sequences. In normal resting conditions, 44.0 ± 4.4% of HR sequences overlapped with CO sequences, suggesting that only around half of the baroreflex HR responses cause CO responses. In HF, HR-LVSP, CO-LVSP, and the HR-CO translation significantly decreased compared with the normal condition (−2.29 ± 0.5 vs. −5.78 ± 0.7 beats·min−1·mmHg−1; −70.95 ± 11.8 vs. −229.89 ± 29.6 ml·min−1·mmHg−1; and 19.66 ± 4.9 vs. 44.0 ± 4.4%, respectively). We conclude that spontaneous baroreflex HR responses do not always cause changes in CO. In addition, HF significantly decreases HR-LVSP, CO-LVSP, and HR-CO translation.

Modulation of spontaneous baroreflex control of heart rate and indexes of vagal tone by passive calf muscle stretch during graded metaboreflex activation in humans

2008 ◽  
Vol 104 (3) ◽  
pp. 716-723 ◽  
Author(s):  
Rachel C. Drew ◽  
Martin P. D. Bell ◽  
Michael J. White
Keyword(s):  
Heart Rate ◽  
Exercise Intensity ◽  
Vagal Tone ◽  
Voluntary Contraction ◽  
Calf Muscle ◽  
Baroreflex Control ◽  
Muscle Metaboreflex ◽  
Spontaneous Baroreflex ◽  
Passive Stretch ◽  
Human Calf

We examined whether spontaneous baroreflex modulation of heart rate and other indexes of cardiac vagal tone could be altered by passive stretch of the human calf muscle during graded concurrent activation of the muscle metaboreflex. Ten healthy subjects performed four trials: a control trial, resting for 1.5 min (0% trial); or 1.5 min of one-legged isometric plantar flexor exercise at 30, 50, and 70% maximal voluntary contraction. The incremental increases in blood pressure (BP) caused were then partially sustained by subsequent local circulatory occlusion (CO). After 3.5 min of CO alone, sustained calf stretch and CO were applied for 3 min. Spontaneous baroreflex sensitivity (SBRS) was progressively decreased with increasing exercise intensity ( P < 0.05). During CO, stretch decreased SBRS and increased BP similarly in all trials ( P < 0.05). Within 15 s of stretch onset, heart rate (HR) increased by 6 ± 1, 6 ± 1, 8 ± 1, and 6 ± 2 beats/min in the 0, 30, 50, and 70% trials, respectively ( P < 0.05), and root mean square of successive differences was decreased from CO-alone levels ( P < 0.05). During the second and third minutes of stretch, HR fell back but remained significantly above CO levels, and common coefficient of variance of R-R interval decreased progressively with increasing prior exercise intensity ( P < 0.05; 70% trial). This suggests that passive stretch of the human calf muscles decreases cardiac vagal outflow irrespective of the levels of BP increase caused by muscle metaboreflex activation and implies that central modulation of baroreceptor input, mediated by the actions of stretch-activated mechanoreceptive muscle afferent fibers, continues.

Spontaneous baroreflex control of heart rate during exercise and muscle metaboreflex activation in heart failure

2007 ◽  
Vol 293 (3) ◽  
pp. H1929-H1936 ◽  
Author(s):  
Ferdinando Iellamo ◽  
Javier A. Sala-Mercado ◽  
Masashi Ichinose ◽  
Robert L. Hammond ◽  
Marco Pallante ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Response Relationship ◽  
Baroreflex Control ◽  
Muscle Metaboreflex ◽  
Stimulus Response ◽  
Spontaneous Baroreflex

In heart failure (HF), there is a reduced baroreflex sensitivity at rest, and during dynamic exercise there is enhanced muscle metaboreflex activation (MRA). However, how the arterial baroreflex modulates HR during exercise is unknown. We tested the hypothesis that spontaneous baroreflex sensitivity (SBRS) is attenuated during exercise in HF and that MRA further depresses SBRS. In seven conscious dogs we measured heart rate (HR), cardiac output, and left ventricular systolic pressure at rest and during mild and moderate dynamic exercise, before and during MRA (via imposed reductions of hindlimb blood flow), and before and after induction of HF (by rapid ventricular pacing). SBRS was assessed by the sequences method. In control, SBRS was reduced from rest with a progressive resetting of the baroreflex stimulus-response relationship in proportion to exercise intensity and magnitude of MRA. In HF, SBRS was significantly depressed in all settings; however, the changes with exercise and MRA occurred with a pattern similar to the control state. As in control, the baroreflex stimulus-response relationship showed an intensity- and muscle metaboreflex (MMR)-dependent rightward and upward shift. The results of this study indicate that HF induces an impairment in baroreflex control of HR at rest and during exercise, although the effects of exercise and MRA on SBRS occur with a similar pattern as in control, indicating the persistence of some vagal activity.

Muscle metaboreflex activation attenuates spontaneous baroreflex control of heart rate during dynamic exercise

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Masashi Ichinose ◽  
Javier A Sala‐Mercado ◽  
Tomoko Ichinose ◽  
Marco Pallante ◽  
Ferdinando Iellamo ◽  
...  
Keyword(s):  
Heart Rate ◽  
Dynamic Exercise ◽  
Baroreflex Control ◽  
Muscle Metaboreflex ◽  
Spontaneous Baroreflex

Assessment of spontaneous baroreflex sensitivity in rats a new method using the concept of statistical dependence

1995 ◽  
Vol 268 (2) ◽  
pp. R382-R388 ◽  
Author(s):  
C. Cerutti ◽  
M. Ducher ◽  
P. Lantelme ◽  
M. P. Gustin ◽  
C. Paultre
Keyword(s):  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
New Method ◽  
Statistical Dependence ◽  
Strongly Correlated ◽  
Vasoactive Drugs ◽  
Hypertensive Rats ◽  
Induced Hypertension ◽  
Spontaneous Baroreflex

A new method was developed to evaluate the cardiac baroreflex sensitivity (BRS) from spontaneous mean arterial pressure (MAP) and heart rate (HR) changes in conscious rats. It relies on the determination of the statistical dependence between MAP and HR values. In 13 control rats, 12 rats with a pharmacologically induced hypertension, and 7 rats with a chronic sinoaortic denervation (SAD), dependent (MAP, HR) couples related to the baroreflex activity were selected to determine the spontaneous BRS (Sp-BRS). In control and hypertensive rats, pharmacological BRS (Ph-BRS) was estimated using graded bolus intravenous doses of vasoactive drugs. Ph-BRS was significantly lower in hypertensive than in control rats. Sp-BRS was determined in 10 control and 10 hypertensive rats and was strongly correlated with Ph-BRS (r = 0.83, n = 20, P < 0.0001). Sp-BRS could be evaluated in six SAD rats and was profoundly decreased (-86%, P < 0.001) compared with control rats. In conclusion, this work validates the estimation of the cardiac BRS from spontaneous MAP and HR variations with use of (MAP, HR) couples of values that are statistically dependent.

scholarly journals Hypertension in Prenatally Undernourished Young-Adult Rats Is Maintained by Tonic Reciprocal Paraventricular–Coerulear Excitatory Interactions

Molecules ◽  
2021 ◽  
Vol 26 (12) ◽  
pp. 3568
Author(s):  
Bernardita Cayupe ◽  
Carlos Morgan ◽  
Gustavo Puentes ◽  
Luis Valladares ◽  
Héctor Burgos ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Young Adult ◽  
Binding Sites ◽  
Systolic Pressure ◽  
Adult Rats ◽  
Excitatory Pathways ◽  
Induced Hypertension ◽  
Prenatal Undernutrition ◽  
Number Of Cells

Prenatally malnourished rats develop hypertension in adulthood, in part through increased α1-adrenoceptor-mediated outflow from the paraventricular nucleus (PVN) to the sympathetic system. We studied whether both α1-adrenoceptor-mediated noradrenergic excitatory pathways from the locus coeruleus (LC) to the PVN and their reciprocal excitatory CRFergic connections contribute to prenatal undernutrition-induced hypertension. For that purpose, we microinjected either α1-adrenoceptor or CRH receptor agonists and/or antagonists in the PVN or the LC, respectively. We also determined the α1-adrenoceptor density in whole hypothalamus and the expression levels of α1A-adrenoceptor mRNA in the PVN. The results showed that: (i) agonists microinjection increased systolic blood pressure and heart rate in normotensive eutrophic rats, but not in prenatally malnourished subjects; (ii) antagonists microinjection reduced hypertension and tachycardia in undernourished rats, but not in eutrophic controls; (iii) in undernourished animals, antagonist administration to one nuclei allowed the agonists recover full efficacy in the complementary nucleus, inducing hypertension and tachycardia; (iv) early undernutrition did not modify the number of α1-adrenoceptor binding sites in hypothalamus, but reduced the number of cells expressing α1A-adrenoceptor mRNA in the PVN. These results support the hypothesis that systolic pressure and heart rate are increased by tonic reciprocal paraventricular–coerulear excitatory interactions in prenatally undernourished young-adult rats.

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.

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