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PubMed2002

Inter-relations among declines in arterial distensibility, baroreflex function and respiratory sinus arrhythmia.

OBJECTIVES: We hypothesized that structural and neural cardiovascular (CV) deficits may be intimately linked. Specifically, decreased carotid distensibility with age may blunt the arterial baroreflex, thereby reducing resting cardiac vagal tone. BACKGROUND: Increased CV risk is associated with lower carotid distensibility, impaired baroreflex function and reduced respiratory sinus arrhythmia (RSA), possibly representing a direct path between structural and neural CV deficits. METHODS: We estimated the mechanostructural and neural components of baroreflex function and examined their relation to RSA in young (20 to 31 years) and older (59 to 71 years) subjects rigorously screened for CV and autonomic diseases. RESULTS: In the older subjects, RSA was < 20% of that in the younger subjects. Moreover, mechanical transduction of pressure into barosensory vessel stretch was approximately 40% lower (p < 0.05) and arterial baroreflex gain more than 60% lower (p < 0.05) in the older group. Although neural transduction of stretch into vagal outflow only tended to be less (p < 0.08), it was an important determinant of baroreflex function. A path analysis model showed comparable contributions of both the mechanical and neural components to baroreflex gain; however, lower overall baroreflex gain in the older group did not relate to lower RSA. CONCLUSIONS: These data suggest that decreased carotid distensibility does reduce baroreflex function with age, but this does not lead to reduced resting vagal outflow.

Adult↗

PubMed1998

Applicability of new techniques in the assessment of arterial baroreflex sensitivity in the elderly: a comparison with established pharmacological methods.

1. There has been considerable interest in techniques recently developed for the study of arterial baroreceptor-cardiac reflex sensitivity based on analysis of spontaneous baroreflex sequences and on spectral analysis. This study examined how these newer techniques agreed with the established pharmacological methods in elderly subjects. 2. In 20 elderly subjects [10 hypertensive (clinic blood pressure 180 +/- 4/88 +/- 2 mmHg) and 10 normotensive (clinic blood pressure 136 +/- 3/73 +/- 2 mmHg)], we assessed baroreflex sensitivity from spontaneous sequences of increasing and decreasing blood pressure and pulse interval and their mean, and from spectral analysis to derive alpha, the index of overall baroreflex gain. Pharmacological baroreflex sensitivity was derived from the blood pressure and pulse interval responses to depressor (sodium nitroprusside) and pressor (phenylephrine) stimuli, and their mean. 3. Baroreflex sensitivity was significantly lower in the hypertensive group by the pharmacological, sequence and spectral methods (all P < 0.05). 4. There was acceptable agreement between pharmacological baroreflex sensitivity and sequences of the same direction, but with some systematic bias. There was also reasonable agreement between pharmacological and spectral baroreflex sensitivity and close agreement without bias between sequence and spectral methods. 5. The newer and established techniques demonstrate acceptable agreement in the elderly, albeit with some systematic bias. Pharmacological methods have enjoyed historical precedence but newer techniques give equivalent results, and are preferable in some circumstances. The newer techniques may be more descriptive of the spontaneous behaviour of the arterial baroreflex at rest rather than under artificially stimulated conditions.

Aged↗

PubMed2001

Comparison of vagal baroreflex function in nonpregnant women and in women with normal pregnancy, preeclampsia, or gestational hypertension.

OBJECTIVE: Our aim was to compare baroreflex function among nonpregnant women and among women with normal pregnancy, preeclampsia, or gestational hypertension. STUDY DESIGN: Baroreflex function was tested in 20 women with preeclampsia, in 20 age- and gestational age-matched normotensive gravid women, in 20 age-matched nonpregnant women, and in 20 nonmatched women with gestational hypertension. The baroreflex was measured by several modalities. RESULTS: Vagal baroreflex gain measured by cross-spectral analysis of parallel spontaneous heart rate and blood pressure changes is significantly decreased in normal pregnancy (15.8 +/- 7.2 vs 10.8 +/- 4.1 ms/mm Hg; P = 0.001), in comparison with vagal baroreflex gain in nonpregnant women. Baroreflex gain is further reduced in preeclamptic pregnancy (10.8 +/- 4.1 vs 7.2 +/- 2.6 ms/mm Hg; P = 0.003) and in gestational hypertension (10.8 +/- 4.1 vs 6.5 +/- 2.7 ms/mm Hg; P = 0.001), compared with that in normal pregnancy. Similar differences were seen with other baroreflex testing modalities. CONCLUSIONS: The normal reduction of baroreflex gain in pregnancy is further depressed in subjects with hypertensive disorders of pregnancy.

Adult↗

PubMed1994

Recovery of attenuated baroreflex sensitivity in conscious dogs after reversal of pacing induced heart failure.

OBJECTIVE: Rapid ventricular pacing reliably induces severe congestive heart failure in dogs, with an associated attenuation of baroreflex sensitivity. Unique to this model is the capacity for rapid recovery of haemodynamics and plasma noradrenaline following the cessation of pacing; however, whether baroreflex sensitivity will similarly recover is unknown. The aims of this study were (1) to assess baroreflex control of heart rate in response to acute hypertensive and hypotensive stimuli during the development of and recovery from severe heart failure, and (2) to correlate baroreflex sensitivity with haemodynamic and echocardiographic indices and with noradrenaline concentrations. METHODS: Serial assessments were performed on six dogs paced to severe heart failure and then allow to recover for four weeks. R-R interval and systolic blood pressure were monitored during administrations of phenylephrine and nitroprusside and the slope (ms.mm Hg-1) of the resultant R-R interval-systolic blood pressure relationship was used to define baroreflex sensitivity. RESULTS: Control phenylephrine and nitroprusside derived slopes were 27.05(SD 7.88) and 17.1(11.03) ms.mm Hg-1 respectively. After one week of pacing the phenylephrine derived slope was unchanged while the nitroprusside slope tended to be attenuated. In severe heart failure, both slopes were severely attenuated, at 1.88(6.45) ms.mm Hg-1 (phenylephrine) and 4.21(3.28) ms.mm Hg-1 (nitroprusside) (both p < 0.05). Intrinsic heart rate, noradrenaline concentrations and cardiac filling pressures were raised at severe heart failure while cardiac output and systolic blood pressure were significantly reduced. Recovery of baroreflex control of heart rate was evident as early as 48 h following pacing cessation and was maintained after four weeks recovery. Haemodynamics, cardiac output, and noradrenaline also returned to control while cardiac dilatation persisted. Nitroprusside and phenylephrine derived slopes were inversely correlated with intrinsic heart rate and pulmonary arterial/capillary wedge pressures respectively. CONCLUSIONS: Despite marked attenuation of baroreflex control of heart rate at severe heart failure, rapid recovery was seen in response to both hypotensive and hypertensive stimuli. The speed with which recovery occurs suggests that attenuation of baroreflex sensitivity at severe heart failure is likely to be mediated by functional alterations rather than morphological damage.

Animals↗

PubMed2003

Effect of systolic blood pressure and carotid stiffness on baroreflex gain in elderly subjects.

BACKGROUND: Aging is associated with diminished baroreflex sensitivity (gain), which predisposes elderly people to orthostatic hypotension, syncope, and cardiovascular morbidity. Aging is also associated with systolic blood pressure (SBP) elevation and carotid artery stiffness, which may both affect baroreflex gain. METHODS: We examined the relation between SBP, carotid artery stiffness, and baroreflex gain in 34 healthy elderly (71 +/- 4 years) and 10 healthy young (31 +/- 3 years) subjects. SBP (Finapres) and carotid artery stiffness (ultrasound measures of relative carotid artery diameter changes during each blood pressure pulse) were measured. The gain of the transfer function relating the R-R interval to SBP fluctuations at a frequency of 0.05-0.15 Hz was used to assess cardiovagal baroreflex gain. RESULTS: Elderly subjects had higher carotid artery stiffness (14.2 +/- 5.1 vs 6.6 +/- 1.8, p <.05), higher SBP (146 +/- 24 vs 125 +/- 8 mmHg, p =.012), and lower baroreflex gain (8.2 +/- 6.4 vs 16.3 +/- 7.4, p <.05) than young subjects. Among all subjects, SBP and carotid artery stiffness both correlated with baroreflex gain (r = -.39, p =.02 for both). Although SBP was related to stiffness across all subjects, this relation was not present among the elderly subjects. Within the elderly group, only SBP was independently related to baroreflex gain (R(2) =.51, p =.009). CONCLUSIONS: SBP elevation in elderly people may affect the neural or cardiac response to blood pressure fluctuations, independent of the mechanical properties of barosensory regions in the carotid artery. Future studies should examine the effect of pharmacologic treatment of hypertension on baroreflex gain in elderly people.

Adult↗

PubMed2003

Hemodilution does not alter arterial baroreflex control of heart rate in anesthetized dogs.

UNLABELLED: The cardiovascular effects of acute normovolemic hemodilution (ANH) are characterized by increased cardiac output and decreased systemic vascular resistance. However, whether arterial baroreflex function is altered by ANH remains undetermined. We assigned 23 anesthetized, mechanically ventilated dogs to mild ANH (hemoglobin, 7-8 g/dL; n = 11) or profound ANH (hemoglobin, 4-5 g/dL; n = 12) achieved by phlebotomy and simultaneous exchange with lactated Ringer's solution at 1:3 ratio to maintain constant central venous pressure and pulmonary artery occluded pressure. Baroreflex sensitivity was assessed by measurements of RR intervals of the electrocardiogram and mean arterial blood pressure (MAP) through a femoral artery catheter. Baroreflex responses were triggered by bolus IV injections of phenylephrine (25-75 micro g) and nitroprusside (50-100 micro g). The linear portion of the baroreflex curves relating RR intervals and MAP were used to determine baroreflex sensitivities. Compared with the predilution period, both ANH groups had significant increases in cardiac output and decreases in systemic vascular resistance (P < 0.01), whereas MAP and heart rate (HR) remained unchanged. However, no significant difference was detected between pre-ANH and post-ANH baroreflex sensitivities in either group. Our results indicate that arterial baroreflex control of HR is preserved during ANH to a hemoglobin concentration of 4-5 g/dL in anesthetized dogs. IMPLICATIONS: Acute normovolemic hemodilution may be preoperatively used to minimize the requirement of allogeneic blood products during major surgery. We found that baroreflex function is preserved during mild (hemoglobin concentration, 7-8 g/dL) and profound hemodilution (hemoglobin concentration, 4-5 g/dL) in pentobarbital-anesthetized dogs.

Anesthesia↗

PubMed1997

Autonomic cardiac regulation in obstructive sleep apnea syndrome: evidence from spontaneous baroreflex analysis during sleep.

OBJECTIVE: To assess spontaneous baroreceptor-heart rate reflex sensitivity during sleep in patients with obstructive sleep apnea syndrome, a condition associated with increased cardiovascular morbidity and mortality and characterized by marked sympathetic activation, which is believed to originate from hypoxic chemoreceptor stimulation, although little is known of other possible mechanisms such as baroreflex impairment. DESIGN AND METHODS: In 11 patients with severe obstructive sleep apnea syndrome (mean+/-SD age 46.8+/-8.1 years, apnea/hypopnea index 67.9+/-19.1 h), who were normotensive or borderline hypertensive during wakefulness by clinic blood pressure measurements, finger blood pressure was monitored beat-by-beat non-invasively (Finapres) at night during polysomnography. Periods of wakefulness and sleep were identified based on electroencephalographic recordings. Baroreflex sensitivity was assessed by the sequence technique, as the slope of the regression line between spontaneous increases or reductions in systolic blood pressure (SBP) and the related lengthening or shortening in the RR interval, occurring over spontaneous sequences of four or more consecutive beats. The number of these sequences was also computed, as an additional index of baroreflex engagement by the spontaneous blood pressure fluctuations. The controls were age-related normotensive or borderline hypertensive subjects without sleep apnea who had been investigated in previous studies; in these subjects blood pressure was recorded intra-arterially over 24 h in ambulatory conditions and spontaneous baroreflex sensitivity was assessed by the sequence technique. RESULTS: In our patients the lowest nocturnal arterial oxygen saturation was 78.6+/-12.1% (mean+/-SD). During sleep, the number of pooled +RR/+SBP and -RR/-SBP sequences per hour was 20.3+/-2.7 per h in patients with sleep apnea and 27.1+/-2.1 /h in controls (means+/-SEM). The average baroreflex sensitivity during sleep periods was 7.04+/-0.8 ms/mmHg in sleep apnea patients and 10.05+/-2.1 ms/mmHg in controls. Both the pooled number of sequences and baroreflex sensitivity values of the sleep apnea patients were significantly (P < 0.01) less than the corresponding night values of control subjects. In the sleep apnea patients, at variance from controls, baroreflex sensitivity did not show any increase during sleep compared with its values during wakefulness (6.9+/-1.0 ms/mmHg). CONCLUSIONS: Our data provide evidence that spontaneous baroceptor reflex sensitivity is depressed in severe obstructive sleep apnea syndrome. This suggests that in such patients baroreflex dysfunction and not only chemoreceptor stimulation by hypoxia may be involved in the sympathetic activation which occurs during sleep. Such dysfunction may contribute to the higher rate of cardiovascular morbidity and mortality reported in these patients.

Adult↗

PubMed1997

Interactions between vasopressin and baroreflex control of the sympathetic nervous system.

1. In addition to its effects at the renal tubules to influence water retention and at vascular smooth muscle to cause vasoconstriction, the hormone arginine vasopressin also appears to modulate cardiovascular reflex control of the sympathetic nervous system. Infusion or endogenous release of vasopressin results in enhanced baroreflex sympatho-inhibitory responses compared with other pressor agents. In addition, when changes in arterial pressure are imposed on an elevated background level of circulating vasopressin, due either to infusion or endogenous release, the arterial baroreflex response is shifted to lower pressures, and the maximum sympatho-excitation to a decrease in pressure is reduced. 2. Evidence suggests that vasopressin may influence cardiovascular reflex function at multiple sites. Nevertheless, the primary site involved in the effects of circulating vasopressin on baroreflex function appears to be in the central nervous system, specifically in the area postrema. Lesion of the area postrema abolishes the ability of circulating vasopressin to modulate arterial baroreflex and cardiopulmonary reflex function and electrical or chemical stimulation of this circumventricular organ mimics the effects of vasopressin. In addition, vasopressin has been shown to influence the activity of area postrema neurons in vivo and in vitro. Although not all studies agree, the effects of the area postrema and vasopressin on cardiovascular reflex function appear to be dependent on afferent input from peripheral baroreceptors. 3. Most evidence suggests that vasopressin exerts its effects on baroreflex function through a V1 vasopressin receptor mechanism. Systemic administration or microinjection into the area postrema of a specific V1 receptor antagonist abolishes the action of arginine vasopressin on arterial baroreflex and cardiopulmonary reflex control of the sympathetic nervous system. 4. The ability of vasopressin and the area postrema to influence baroreflex function appears to be dependent on an alpha 2-adrenoceptor mechanism at the level of the nucleus tractus solitarius (NTS). Blockade of alpha 2-adrenoceptors in the NTS abolishes the effects of vasopressin and the area postrema on the sympathetic nervous system. Facilitation of NTS processing of baroreceptor afferent inputs by the area postrema could contribute to the enhanced sympatho-inhibition and shift of the baroreflex curve to lower pressures during elevations in circulating vasopressin.

Afferent Pathways↗

PubMed2001

Effects of exercise pressor reflex activation on carotid baroreflex function during exercise in humans.

1. This investigation was designed to determine the contribution of the exercise pressor reflex to the resetting of the carotid baroreflex during exercise. 2. Ten subjects performed 3.5 min of static one-legged exercise (20 % maximal voluntary contraction) and 7 min dynamic cycling (20 % maximal oxygen uptake) under two conditions: control (no intervention) and with the application of medical anti-shock (MAS) trousers inflated to 100 mmHg (to activate the exercise pressor reflex). Carotid baroreflex function was determined at rest and during exercise using a rapid neck pressure/neck suction technique. 3. During exercise, the application of MAS trousers (MAS condition) increased mean arterial pressure (MAP), plasma noradrenaline concentration (dynamic exercise only) and perceived exertion (dynamic exercise only) when compared to control (P < 0.05). No effect of the MAS condition was evident at rest. The MAS condition had no effect on heart rate (HR), plasma lactate and adrenaline concentrations or oxygen uptake at rest and during exercise. The carotid baroreflex stimulus-response curve was reset upward on the response arm and rightward to a higher operating pressure by control exercise without alterations in gain. Activation of the exercise pressor reflex by MAS trousers further reset carotid baroreflex control of MAP, as indicated by the upward and rightward relocation of the curve. However, carotid baroreflex control of HR was only shifted rightward to higher operating pressures by MAS trousers. The sensitivity of the carotid baroreflex was unaltered by exercise pressor reflex activation. 4. These findings suggest that during dynamic and static exercise the exercise pressor reflex is capable of actively resetting carotid baroreflex control of mean arterial pressure; however, it would appear only to modulate carotid baroreflex control of heart rate.

Adult↗

PubMed1993

The neuropeptide CRF is involved in the modulation of the baroreflex during hindlimb ischaemia in the anaesthetized rat.

1. The effects of bilateral hindlimb ischaemia (BHLI), and of administration of the neuropeptide corticotrophin-releasing factor (CRF), were tested on cardiovascular variables in propofol-anaesthetized Sprague-Dawley rats. In addition, the effects of antagonizing endogenous CRF on the cardiovascular response to BHLI was investigated. 2. BHLI produced significant increases in mean arterial pressure and heart rate. Baroreflex sensitivity was reduced in all animals tested both 10 and 30 min after the induction of ischemia and this was accompanied by changes which are consistent with an underlying baroreflex resetting. 3. Intracerebroventricular (I.C.V.) administration of CRF (1.5 nmol) produced significant increases in heart rate but not mean arterial pressure. CRF also produced significant reductions in baroreflex sensitivity 10 and 30 min after administration, but there was no consistent evidence of baroreflex resetting. These effects of CRF could be prevented by pretreatment with the synthetic CRF antagonist, alpha-helical CRF(9-41) (alpha hCRF, 6.5 nmol, I.C.V.), which itself had no effect on these cardiovascular variables. 4. Pretreatment with alpha hCRF (6.5 nmol, I.C.V.) prevented the reduction in baroreflex sensitivity observed 10 min after the induction of BHLI, but had no consistent effect on the pressor or tachycardiac responses to BHLI and allowed a clear expression of BHLI-induced baroreflex resetting. alpha-Helical CRF(9-41) had no effect on the reduction in baroreflex sensitivity after 30 min of BHLI. 5. We conclude that corticotrophin-releasing factor mediates, at least in part, the early reduction in baroreflex sensitivity observed during hindlimb ischaemia in the rat.

Anesthesia↗

PubMed2003

Partial blockade of skeletal muscle somatosensory afferents attenuates baroreflex resetting during exercise in humans.

During exercise, the carotid baroreflex is reset to operate around the higher arterial pressures evoked by physical exertion. The purpose of this investigation was to evaluate the contribution of somatosensory input from the exercise pressor reflex to this resetting during exercise. Nine subjects performed seven minutes of dynamic cycling at 30% of maximal work load and three minutes of static one-legged contraction at 25% maximal voluntary contraction before (control) and after partial blockade of skeletal muscle afferents with epidural anaesthesia. Carotid baroreflex function was assessed by applying rapid pulses of hyper- and hypotensive stimuli to the neck via a customised collar. Using a logistic model, heart rate (HR) and mean arterial pressure (MAP) responses to carotid sinus stimulation were used to develop reflex function stimulus-response curves. Compared with rest, control dynamic and static exercise reset carotid baroreflex-HR and carotid baroreflex-MAP curves vertically upward on the response arm and laterally rightward to higher operating pressures. Inhibition of exercise pressor reflex input by epidural anaesthesia attenuated the bi-directional resetting of the carotid baroreflex-MAP curve during both exercise protocols. In contrast, the effect of epidural anaesthesia on the resetting of the carotid baroreflex-HR curve was negligible during dynamic cycling whereas it relocated the curve in a laterally leftward direction during static contraction. The data suggest that afferent input from skeletal muscle is requisite for the complete resetting of the carotid baroreflex during exercise. However, this neural input appears to modify baroreflex control of blood pressure to a greater extent than heart rate.

Adult↗

PubMed2005

Human vagal baroreflex sensitivity fluctuates widely and rhythmically at very low frequencies.

Arterial pressure fluctuates rhythmically in healthy supine resting humans, who, from all outward appearances, are in a 'steady-state'. Others have asked, If baroreflex mechanisms are functioning normally, how can arterial pressure be so variable? We reanalysed data from nine healthy young adult men and women and tested the hypotheses that during brief periods of observation, human baroreflex sensitivity fluctuates widely and rhythmically. We estimated vagal baroreflex sensitivity with systolic pressure and R-R interval cross-spectra measured over 15 s segments, moved by 2 s steps through 20-min periods of frequency- and tidal volume-controlled breathing. We studied each subject at the same time on three separate days, with fixed protocols that included two physiological states, supine and passive 40 deg upright tilt, before and after beta-adrenergic, cholinergic, and angiotensin converting enzyme blockade. Minimum, mean and maximum (+/-s.d.) supine control baroreflex sensitivities averaged 5 +/- 3, 18 +/- 6, and 55 +/- 22 ms mmHg(-1). In most subjects, moderate ongoing fluctuations of baroreflex sensitivity were punctuated by brief major peaks, yielding frequency distributions that were skewed positively. Fast Fourier transforms indicated that baroreflex sensitivity fluctuations (expressed as percentages of total power) concentrated more in very low, 0.003-0.04 Hz, than ultra low, 0.0-0.003 Hz, frequencies (77 +/- 7 versus 11 +/- 8%, P < or = 0.001, rank sum test). Autoregressive centre frequencies averaged 0.012 +/- 0.003 Hz. The periodicity of very low frequency baroreflex sensitivity fluctuations was not influenced significantly by upright tilt, or by variations of autonomic drive or angiotensin activity. Our analysis indicates that during ostensibly 'steady-state' conditions, human vagal baroreflex sensitivity fluctuates in a major way, at very low frequencies.

Adrenergic beta-Agonists↗

PubMed2002

Reduced cardiovagal baroreflex gain in visceral obesity: implications for the metabolic syndrome.

The influence of excess total and abdominal adiposity on cardiovagal baroreflex gain remains unclear. We tested the hypotheses that cardiovagal baroreflex gain would be reduced in men with 1) higher [higher fat (HF), mass >20 kg, n = 11] compared with lower [lower fat (LF), mass <20 kg, n = 10] levels of total body and abdominal fat and 2) higher abdominal visceral fat (HAVF; n = 10) compared with total body weight- and subcutaneous fat-matched peers with lower abdominal visceral fat (LAVF; n = 7) levels. To accomplish this, we measured cardiovagal baroreflex gain (modified Oxford technique), body composition (dual energy X-ray absorptiometry), and abdominal visceral and subcutaneous fat (computed tomography) in sedentary men (age, 18-40 yr; body mass index, <34.9 kg/m(2)) across a wide range of adiposity. Cardiovagal baroreflex gain was significantly lower in HF compared with LF (14.3 +/- 2.8 vs. 21.4 +/- 2.8 ms/mmHg, respectively). In addition, cardiovagal baroreflex gain was lower in HAVF compared with LAVF (13.0 +/- 2.0 vs. 21.4 +/- 3.6 ms/mmHg, P < 0.05). Therefore, the results of the present study indicate that cardiovagal baroreflex gain is reduced in men with elevated total body and abdominal fat mass. The reduced cardiovagal baroreflex gain in these individuals appears to be linked to their higher level of abdominal visceral fat. Importantly, reduced cardiovagal baroreflex gain may contribute to the increased risk of cardiovascular disease observed in men with the metabolic syndrome.

Abdomen↗

PubMed1993

Carotid baroreflex responsiveness during dynamic exercise in humans.

We utilized 5-s changes of neck pressure and neck suction (from 40 to -80 Torr) to alter carotid sinus transmural pressure in seven men with peak oxygen uptake (VO2peak) of 41.4 +/- 3.6 ml O2.kg-1.min-1. Peak responses of heart rate (HR) and mean arterial pressure (MAP) to each carotid sinus perturbation were used to construct open-loop baroreflex curves at rest and during exercise at 25.7 +/- 1.1 and 47.4 +/- 1.9% VO2peak. The baroreflex curves were fit to a logistic function describing the sigmoidal nature of the carotid sinus baroreceptor reflex. Maximal gain for baroreflex control of HR (-0.31 +/- 0.05 beats.min-1.mmHg-1) and MAP (-0.30 +/- 0.08 mmHg/mmHg) at rest was the same as during exercise at 25 and 50% VO2peak (-0.30 +/- 0.05, -0.39 +/- 0.13 beats.min-1.mmHg-1 for HR, P = NS; -0.23 +/- 0.04, -0.60 +/- 0.38 mmHg/mmHg for MAP, P = NS). Resetting of the baroreflex occurred during exercise at 50% VO2peak. The centering point, threshold, and saturation pressures were significantly increased for baroreflex control of HR (delta pressure = 26.3 +/- 6.8, 19.6 +/- 10.4, 33.0 +/- 5.6 mmHg, P < 0.05) and MAP (delta pressure = 27.1 +/- 7.7, 16.1 +/- 14.8, 38.2 +/- 8.5 mmHg, P < 0.05). The operating point (steady-state HR and MAP) was shifted closer to threshold of the baroreflex during exercise at 50% VO2peak, as reflected by differences in HR and MAP between the centering and operating points (delta HR = 12.5 +/- 4.7 beats/min, P = 0.10; delta MAP = 7.6 +/- 1.3 mmHg, P < 0.05). These findings suggest a resetting of the carotid baroreflex during exercise with no attenuation in maximal sensitivity. A shift in operating point toward threshold of the baroreflex enables effective buffering of elevations in systemic blood pressure via reflex alterations in HR and MAP.

Adolescent↗

PubMed1994

Dynamic arterial baroreflex in rabbits with heart failure induced by rapid pacing.

Excessive sympathetic nerve activity in heart failure could be attributable to impaired arterial baroreflex function. Employing transfer function analysis, we evaluated the arterial baroreflex in control rabbits (n = 8) and in rabbits with rapid pacing-induced heart failure (n = 10) in a dynamic manner. Rabbits in the heart-failure group showed elevated filling pressures, depressed first derivative of left ventricular pressure, pulmonary congestion, and an increased level of plasma norepinephrine. Varying aortic pressure pseudorandomly and recording responses in renal nerve activity, we calculated the transfer function from aortic pressure to renal nerve activity. The gain of the transfer function was similar between control and heart-failure rabbits over 0.04-0.4 Hz as well as the phase and the coherence, indicating that the dynamic arterial baroreflex was preserved in our rabbit heart-failure model. Vagotomy increased the gain of the arterial baroreflex over 0.04-0.4 Hz in control (P < 0.05) but not in heart-failure rabbits, indicating that vagal afferents, which normally inhibit the dynamic arterial baroreflex, no more did so in heart failure. We conclude that excessive sympathetic nerve activity in heart failure may not be due to impaired dynamic arterial baroreflex, but that this apparently preserved arterial baroreflex in heart failure may be due to impaired cardiopulmonary baroreflex.

Animals↗

PubMed1995

A single bout of exhaustive exercise affects integrated baroreflex function after 16 days of head-down tilt.

We tested the hypothesis that one bout of maximal exercise performed 24 h before reambulation from 16 days of 6 degrees head-down tilt (HDT) could increase integrated baroreflex sensitivity. Isolated carotid-cardiac and integrated baroreflex function was assessed in seven subjects before and after two periods of HDT separated by 11 mo. On the last day of one HDT period, subjects performed a single bout of maximal cycle ergometry (exercise). Subjects did not exercise after the other HDT period (control). Carotid-cardiac baroreflex sensitivity was evaluated using a neck collar device. Integrated baroreflex function was assessed by recording heart rate (HR) and blood pressure (MAP) during a 15-s Valsalva maneuver (VM) at a controlled expiratory pressure of 30 mmHg. The ratio of change in HR to change in MAP (delta HR/ delta MAP) during phases II and IV of the VM was used as an index of cardiac baroreflex sensitivity. Baroreflex-mediated vasoconstriction was assessed by measuring the late phase II rise in MAP. Following HDT, carotid-cardiac baroreflex sensitivity was reduced (2.8 to 2.0 ms/mmHg; P = 0.05) as was delta HR/ delta MAP during phase II (-1.5 to -0.8 beats/mmHg; P = 0.002). After exercise, isolated carotid baroreflex activity and phase II delta HR/ delta MAP returned to pre-HDT levels but remained attenuated in the control condition. Phase IV delta HR/ delta MAP was not altered by HDT or exercise. The late phase II increase of MAP was 71% greater after exercise compared with control (7 vs. 2 mmHg; P = 0.041).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1996

Arginine vasopressin modulation of arterial baroreflex responses in fetal and newborn sheep.

The present study was designed to test the hypothesis that the influence of circulating vasopressin (AVP) on the arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR) changes during development. To test this hypothesis, we studied arterial baroreflex-mediated control of HR and RSNA in the presence of increasing plasma levels of AVP in conscious, chronically instrumented fetal, newborn, and adult sheep. In fetal and newborn sheep, increasing plasma AVP levels (from < 10 to > 200 microU/ml) increased resting levels of mean arterial blood pressure (MABP) and decreased HR and RSNA. HR and RSNA baroreflex responses to variations of MABP with nitroprusside and phenylephrine infusion were not modified by elevated AVP levels in either newborn or fetal sheep, except for a small decrease in maximal HR response to nitroprusside infusion in the newborn animals. In contrast, in adults, AVP caused bradycardia and a decrease in RSNA without change in MABP, accompanied by resetting of the arterial baroreflex (decrease in maximal HR and RSNA, decrease in RSNA gain, and shift of HR to lower pressure). To test the hypothesis that the inability of AVP to reset the arterial baroreflex early during development was not secondary to maximal stimulation of V1 receptors during baseline conditions, we investigated the effect of V1-receptor blockade on baseline cardiovascular and arterial baroreflex function in newborn lambs. Administration of a V1-receptor antagonist produced no significant changes in resting MABP, HR, and RSNA and did not influence arterial baroreflex-mediated changes in HR and RSNA. These results indicate that, contrary to adults, circulating AVP does not modulate the arterial baroreflex in fetal and newborn sheep.

Animals↗

PubMed1998

Attenuated baroreflex control of sympathetic nerve activity after cardiovascular deconditioning in rats.

The effect of cardiovascular deconditioning on baroreflex control of the sympathetic nervous system was evaluated after 14 days of hindlimb unloading (HU) or the control condition. Rats were chronically instrumented with catheters and sympathetic nerve recording electrodes for measurement of mean arterial pressure (MAP) and heart rate (HR) and recording of lumbar (LSNA) or renal (RSNA) sympathetic nerve activity. Experiments were conducted 24 h after surgery, with the animals in a normal posture. Baroreflex function was assessed using a logistic function that related HR and LSNA or RSNA to MAP during infusion of phenylephrine and nitroprusside. Baroreflex influence on HR was not affected by HU. Maximum baroreflex-elicited LSNA was significantly reduced in HU rats (204 +/- 11.9 vs. 342 +/- 30.6% baseline LSNA), as was maximum reflex gain (-4.0 +/- 0.6 vs. -7.8 +/- 1.3 %LSNA/mmHg). Maximum baroreflex-elicited RSNA (259 +/- 10.8 vs. 453 +/- 28.0% baseline RSNA), minimum baroreflex-elicited RSNA (-2 +/- 2.8 vs. 13 +/- 4.5% baseline RSNA), and maximum gain (-5.8 +/- 0.5 vs. -13.6 +/- 3.1 %RSNA/mmHg) were significantly decreased in HU rats. Results demonstrate that baroreflex modulation of sympathetic nervous system activity is attenuated after cardiovascular deconditioning in rodents. Data suggest that alterations in the arterial baroreflex may contribute to orthostatic intolerance after a period of bedrest or spaceflight in humans.

Animals↗