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At least 433 records · Page 24Linked to original sources
PubMed2005

Neural activity of the cardiac baroreflex decreases with age in normotensive and hypertensive subjects.

OBJECTIVES: Baroreflex control of the heart rate is impaired in hypertensive subjects and decreases with age. The decrease in cardiac baroreflex sensitivity (BRS) is often ascribed to decreased distension of the pressure-sensing arterial wall segments. However, alterations in the sensing and processing of neural signals may be involved as well. DESIGN: Conventionally, both vessel wall stiffness and the sensing and neural processing of the baroreflex are incorporated in the measure of pressure-derived BRS. We introduce stretch-derived BRS, which only considers the sensing and neural components of the baroreflex. METHODS: To determine stretch-derived BRS in a non-invasive manner, we measured the spontaneously occurring low-frequency variations (range, 0.06-0.12 Hz) in the carotid artery diameter and the corresponding R-R interval fluctuations, and determined the associated transfer function. The stretch-derived BRS in a group of age-matched (age range, 25-72 years) normotensive (n = 20) and hypertensive (n = 21) subjects was compared. RESULTS: In both subject groups the stretch-derived BRS decreased significantly with age. Moreover, the stretch-derived BRS of both groups was only different below 50 years of age. CONCLUSIONS: The analysis of low-frequency fluctuations in the carotid artery diameter demonstrates that aging as well as hypertension are associated with impaired neural control of the baroreflex. Beyond 50 years of age the effect of hypertension cannot be distinguished from the effect of aging.

Adult↗
PubMedDate not supplied

Heart rate variability biofeedback increases baroreflex gain and peak expiratory flow.

OBJECTIVE: We evaluated heart rate variability biofeedback as a method for increasing vagal baroreflex gain and improving pulmonary function among 54 healthy adults. METHODS: We compared 10 sessions of biofeedback training with an uninstructed control. Cognitive and physiological effects were measured in four of the sessions. RESULTS: We found acute increases in low-frequency and total spectrum heart rate variability, and in vagal baroreflex gain, correlated with slow breathing during biofeedback periods. Increased baseline baroreflex gain also occurred across sessions in the biofeedback group, independent of respiratory changes, and peak expiratory flow increased in this group, independently of cardiovascular changes. Biofeedback was accompanied by fewer adverse relaxation side effects than the control condition. CONCLUSIONS: Heart rate variability biofeedback had strong long-term influences on resting baroreflex gain and pulmonary function. It should be examined as a method for treating cardiovascular and pulmonary diseases. Also, this study demonstrates neuroplasticity of the baroreflex.

Adult↗
PubMed2007

Contribution of imidazoline receptors and alpha2-adrenoceptors in the rostral ventrolateral medulla to sympathetic baroreflex inhibition by systemic rilmenidine.

OBJECTIVES: To determine whether the hypotensive and sympathetic baroreflex inhibition by rilmenidine administered systemically are mediated via imidazoline receptors in the rostral ventrolateral medulla (RVLM). METHODS: Initial dose-response curves to rilmenidine were determined in urethane anaesthetized rabbits. Effects of a single intravenous dose of rilmenidine (445 microg/kg) on the renal sympathetic nerve activity (RSNA) baroreflex were examined before and after microinjection into the RVLM of the mixed imidazoline/alpha2-adrenoceptor antagonist idazoxan and the alpha2-adrenoceptor antagonist 2-methoxyidazoxan (2-MI). RESULTS: Intravenous administration of rilmenidine lowered mean arterial pressure and RSNA, inhibited the RSNA baroreflex range by 33% and shifted the baroreflex curve to the left. Idazoxan injected into the RVLM reversed the hypotension and completely restored the baroreflex curve at doses that did not affect the hypotension produced by the selective alpha2-adrenoceptor agonist alpha-methylnoradrenaline. The alpha2-adrenoceptor antagonist, 2-MI also reversed the rilmenidine sympatho-inhibition suggesting that alpha2-adrenoceptors are activated as well. CONCLUSIONS: The results of the present study show that the hypotensive and sympatho-inhibitory actions of systemic rilmenidine are primarily mediated via imidazoline receptors in the RVLM. However, alpha2-adrenoceptors are also involved, probably as a direct result of the imidazoline receptor action.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1993

Effects of high salt intake on control of hindlimb vascular resistance by arterial baroreflex and vagal afferents in spontaneously hypertensive rats.

1. This study aimed to examine whether a high salt diet alters control of vascular resistance by arterial baroreflex and vagal afferents in spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). 2. SHR and WKY aged 8 weeks were fed either high (8%) or normal salt (0.4%) diet for 4 weeks. Arterial baroreflex control of hindlimb vascular resistance was assessed by examining reflex-induced vasodilation and vasoconstriction in response to phenylephrine and nitroprusside, respectively, in the constant-flow perfused hindlimb of urethane-anesthetized rats. 3. Tonic influence of the cardiopulmonary vagal afferents was evaluated by examining the effects of vagotomy on hindlimb vascular resistance and on the gain of arterial baroreflex control of hindlimb vascular resistance. 4. The gain of the arterial baroreflex control of hindlimb vascular resistance in response to both phenylephrine and nitroprusside were not significantly different between SHR receiving high and normal salt diets, and between WKY receiving high and normal salt diets. 5. Vagotomy increased hindlimb vascular resistance in all four groups of rats. However the high salt diet than those in SHR on a normal salt diet but similar between the two groups of WKY. Vagotomy increased the slope of arterial baroreflex control of hindlimb vascular resistance in SHR receiving a normal salt diet and the two groups of WKY but not in SHR receiving a high salt diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMedDate not supplied

Baroreflex control of coronary blood flow varies regionally in awake dogs.

1. Baroreflex responses to changes in aortic pressure were measured simultaneously in three main coronary regions of awake dogs. 2. Pulsed Doppler flow probes were mounted at prior surgery on the right, circumflex and anterior descending coronary arteries; the animals were placed in complete heart block and the left ventricle was paced. After 2-4 weeks recovery, baroreflexes were evoked by inflating a balloon catheter placed in the mid-thoracic aorta via the femoral arteriotomy. Flow and pressure data were collected at rest, and during acute (8s) and steady-state (25s) baroreflex challenge. 3. Changing ventricular rate alone caused a fall in aortic pressure at low rates; however, over the range 60 to 180 b.p.m., circumflex and anterior descending coronary flow and conductance changed directly with ventricular rate, but right coronary flow and conductance remained unchanged. 4. Acute aortic pressure elevation increased flow at 8s in all beds at all rates. Conductance effects at 60 b.p.m. were negligible in all three beds, but rose at 100 and 180 b.p.m. in the right and circumflex beds. 5. Sustained aortic pressure elevation (25s) caused flow to return towards control in all beds ventricular rates, but in the right coronary at 60 b.p.m. flow fell below control. Conductance at this time was unchanged at all rates in the anterior descending bed, fell modestly in the circumflex, and decreased to below resting in the right coronary bed. 6. Baroreflex control of coronary flow and conductance thus varies between territories, and within territories, depending on ventricular rate. The right coronary bed appears to be regulated by a bidirectional, baroreflex-linked mechanism, which is functionally opposite in action to that found in most vascular beds.

Animals↗
PubMed1995

Assessment of baroreflex control from beat-to-beat blood pressure and heart rate changes: a validation study.

In this study, we tested the validity of a new method designed to estimate baroreflex control of heart rate from spontaneous changes in systolic pressure and pulse interval. This method was compared with a conventional method of assessing baroreflex control through measuring reflex adjustments in pulse interval associated with pharmacological manipulations of blood pressure. The estimates of baroreflex control derived from the two methods were significantly correlated; however, only the estimate derived using pharmacological changes in pressure detected significant impairment of baroreflex control in patients with damage to baroafferents produced by radiation for oropharyngeal cancer. Analysis of spontaneous changes in pressure and pulse interval therefore provide a meaningful estimate of baroreflex control of heart rate that is, however, less sensitive than estimates obtained using pharmacological manipulations in pressure.

Adult↗
PubMed1998

Baroreflex sensitivity and heart rate variability in coronary disease compared to dilated cardiomyopathy.

This study was designed to compare baroreceptor sensitivity and heart rate variability as measures of cardiac autonomic tone in patients with coronary disease (CAD, n = 49) and idiopathic dilated cardiomyopathy (IDC, n = 130). Time domain heart rate variability, including SDNN, SDANN, and pNN50, was determined during 24-hour Holter ECG. Baroreflex sensitivity was analyzed nonivasively using the phenylephrine method. Baroreflex sensitivity and heart rate variability were comparable between patients with CAD versus IDC (baroreflex sensitivity: 6.1 +/- 3 vs 6.9 +/- 5 ms/mmHg; SDNN: 97 +/- 40 vs 114 +/- 41 ms; SDANN: 83 +/- 33 vs 99 +/- 41 ms; pNN50: 3.9 +/- 4 vs 9.6 +/- 13 ms, P = NS for all comparisons). Likewise, a subgroup analysis of patients with a left ventricular ejection fraction (LVEF) < or = 30% showed no significant difference in baroreceptor sensitivity and heart rate variability between IDC and CAD patients. Patients with CAD and an LVEF > 30% had a decreased heart rate variability but not a decreased baroreflex sensitivity compared to patients with IDC and LVEF > 30% (baroreflex sensitivity: 6.4 +/- 4 vs 8.3 +/- 6 ms/mmHg, P = NS; SDNN: 98 +/- 19 vs 128 +/- 42 ms, P < 0.05; SDANN: 86 +/- 21 vs 112 +/- 43 ms, P < 0.05; pNN50: 4.2 +/- 3 vs 12.3 +/- 8 ms, P < 0.05). Patients with a markedly depressed LVEF show comparable alterations in cardiac autonomic tone whether they have CAD or IDC. Patients with CAD and preserved LV function, however, have a decreased heart rate variability compared to patients with IDC and preserved LV function. The prognostic significance of these findings will be determined prospectively in a large patient cohort at our institution.

Baroreflex↗
PubMed1993

Noradrenaline contributes to modulation of the carotid sinus baroreflex in the nucleus tractus solitarii area in the rabbit.

The authors examined the contribution of the noradrenergic system to central cardiovascular regulation in the dorso-medial region of the medulla oblongata, including the nucleus tractus solitarii (NTS) area, in anaesthetized rabbits. First, to determine the modulation of the carotid sinus baroreflex system by alpha-blocker, which blocks the action of noradrenaline, the open loop relationship between isolated carotid sinus pressure (CSP) and renal nerve activity (RNA) was examined before and after injection of alpha-blocker (phentolamine, 10 micrograms, bilateral). alpha-Blocker injected to the NTS area caused a decrease in RNA at low CSP level (40-50 mmHg), and RNA response remained higher at high CSP levels (130 mmHg), in comparison with control. Baroreflex sensitivity was attenuated significantly from 10.9 +/- 2.2 to 5.0 +/- 0.5% (mmHg-1). The data show that the NTS area is one of the important sites in central modulation of the carotid sinus baroreflex function. It is suggested that the noradrenergic system in the NTS area contributed to facilitating carotid sinus baroreflex function. Second, using the dialysis technique, a dialysis probe was implanted in the dorso-medial region of the medulla oblongata, including the NTS area, and perfused with Ringer's solution. Dialysates were collected from this region and noradrenaline (NA) output was determined by high-performance liquid chromatography/electrochemical methods. Drug-induced hypotension caused a 30% decrease in arterial pressure and an increase in dialysate NA levels from 6.8 +/- 0.2 to 9.0 +/- 0.4 pg sample-1. The results show that noradrenaline in the NTS area is involved in the regulation of arterial pressure through the central modulation of arterial baroreflex function.

Animals↗
PubMed1994

Facilitation of the arterial baroreflex by the ventrolateral part of the midbrain periaqueductal grey matter in rats.

1. The effects of stimulation of the ventrolateral part of the midbrain periaqueductal grey matter (PAG) on the arterial baroreflex were investigated in urethane-chloralose anaesthetized and artificially ventilated rats. 2. Both electrical and chemical stimulation of the ventrolateral PAG provoked hypotension, vagal bradycardia and marked facilitation of baroreflex vagal bradycardia (BVB), which was induced by stimulation of the aortic depressor nerve. The magnitude of ventrolateral PAG facilitation of BVB was 328 +/- 193% (n = 34) for electrical stimulation and 243 +/- 224% (n = 13) for chemical stimulation. Baroreflex hypotension was slightly augmented during either electrical or chemical stimulation of the ventrolateral PAG in vagotomized rats. 3. Stimulation of the nucleus raphe magnus (NRM) also provoked hypotension, vagal bradycardia and facilitation of BVB. The magnitude of BVB facilitation was 234 +/- 132% (n = 8) for electrical stimulation and 328 +/- 170% (n = 7) for chemical stimulation. After microinjection of kainic acid into the NRM region, baroreflex facilitation, as well as hypotension and vagal bradycardia, produced by ventrolateral PAG stimulation, was almost abolished. 4. In conclusion, the ventrolateral PAG, besides producing hypotension and bradycardia, facilitates arterial baroreflexes. These effects are exerted via the NRM, sharply contrasting with effects of the dorsal PAG.

Animals↗
PubMed2004

Acute shifts in baroreflex control of renal sympathetic nerve activity induced by REM sleep and grooming in rats.

The present study aimed to determine the impact of REM sleep and grooming on the baroreflex stimulus-response curve for renal sympathetic nerve activity (RSNA). At least 3 days before study, Wistar female rats (n= 12) were chronically implanted with catheters to measure systemic arterial pressure (P(a)) and to intravenously infuse vasoactive drugs. In addition, electrodes were placed for measurements of RSNA, electroencephalogram, trapezius electromyogram and electrocardiogram. The baroreflex curve for RSNA was determined by changing P(a) using rapid intravenous infusions of phenylephrine and nitroprusside and then fitted to an inverse sigmoid function curve. REM sleep induced a vertical suppression of the P(a)-RSNA baroreflex curve, which was characterized by significant decreases in the maximum response (by 72.0%, P < 0.05) and the maximum gain (by 4.02% mmHg(-1), P < 0.05) compared with NREM sleep level. Grooming shifted the P(a)-RSNA baroreflex curve upward and to the right, which was associated with increases in the maximum response (by 45.2%, P < 0.05), the minimum response (by 20.7%, P < 0.05) and the pressure at the centering point (by 11.1 mmHg, P < 0.05). These data suggest that the P(a)-RSNA baroreflex curve was shifted acutely and differently in a state-dependent manner during natural sleep and wake cycle in rats.

Adrenergic Fibers↗
PubMed2005

Reduced alpha-adrenoceptor responsiveness and enhanced baroreflex sensitivity in Cry-deficient mice lacking a biological clock.

To reveal the role of clock genes in generating the circadian rhythm of baroreflexes, we continuously measured mean arterial pressure and baroreflex sensitivity in free-moving normal wild-type mice, and in Cry-deficient mice which lack a circadian rhythm, in constant darkness for 24 h. In wild-type mice the mean arterial pressure was higher at night than during the day, and was accompanied by a significantly enhanced baroreflex sensitivity of -13.6 +/- 0.8 at night compared with -9.7 +/- 0.7 beats min(-1) mmHg(-1) during the day (P < 0.001). On the other hand, diurnal changes in arterial pressure disappeared in Cry-deficient mice with remarkably enhanced baroreflex sensitivity compared with wild-type mice (P < 0.001): -21.9 +/- 1.6 at night and -23.1 +/- 2.1 beats min(-1) mmHg(-1) during the day. Moreover, the mean arterial pressure response to 10 microg kg(-1) of phenylephrine, an alpha1-adrenoceptor agonist, was severely suppressed in Cry-deficient mice regardless of time, while that for the wild-type mice was 10.1 +/- 1.9 mmHg in the night, significantly lower than 22.0 +/- 3.5 mmHg in the day (P < 0.01). These results suggest that CRY genes are involved in generating the circadian rhythm of baroreflex sensitivity, partially by regulating alpha(1)-adrenoceptor-mediated vasoconstriction in peripheral vessels.

Adrenergic alpha-Agonists↗
PubMed2006

Disinhibition of the cardiac limb of the arterial baroreflex in rat: a role for metabotropic glutamate receptors in the nucleus tractus solitarii.

The nucleus tractus solitarii (NTS) is the first site of integration for primary baroreceptor afferents, which release glutamate to excite second-order neurones through ionotropic receptors. In vitro studies indicate that glutamate may also activate metabotropic receptors (mGluRs) to modulate the excitability of NTS neurones at pre- and postsynaptic loci. We examined the functional role of metabotropic glutamate receptors (mGluRs) in modulating the baroreceptor reflex in the rat NTS. Using the working heart-brainstem preparation, the baroreflex was activated using brief pressor stimuli and the consequent cardiac (heart rate change) and non-cardiac sympathetic (T8-10 chain) baroreflex gains were obtained. Microinjections of glutamate antagonists were made bilaterally into the NTS at the site of termination of baroreceptor afferents. NTS microinjection of kynurenate (ionotropic antagonist) inhibited both the cardiac and sympathetic baroreflex gains (16 +/- 5% and 59 +/- 11% of control, respectively). The non-selective mGluR antagonist MCPG produced a dose-dependent inhibition of the cardiac gain (30 +/- 3% of control) but not the sympathetic gain. Selective inhibitions of the cardiac gain were also seen with LY341495 and EGLU suggesting the response was mediated by group II mGluRs. This effect on cardiac gain involves attenuation of the parasympathetic baroreflex as it persists in the presence of atenolol. Prior NTS microinjection of bicuculline (GABA(A) antagonist) prevented the mGluR-mediated attenuation of the cardiac gain. These results are consistent with the reported presynaptic inhibition of GABAergic transmission by group II mGluRs in the NTS and constitute a plausible mechanism allowing selective feed-forward disinhibition to increase the gain of the cardiac limb of the baroreflex without changing the sympathoinhibitory component.

Animals↗
PubMed1997

Assessment of spontaneous baroreflex sensitivity in neonates.

AIMS: To determine whether it is possible to assess baroreflex sensitivity in neonates by studying only spontaneous variation in systolic blood pressure and heart rate. METHODS: ECG and non-invasive blood pressure signals were continuously studied in 14 preterm neonates (term 29-32 weeks) and five term neonates (term 40-41 weeks). Non-invasive blood pressure measures were obtained using a Finapres placed around the child's wrist. Both signals (ECG and blood pressure), sampled at 400 Hz, were digitised by an A/D converter and stored in a binary mode on magnetic disk. An inhouse software QRS detection algorithm was used to define R peaks of the QRS complexes with an accuracy greater than 2 ms. Four 4 minute periods were recorded in each infant. The slope of the linear regression of RR intervals versus systolic blood pressure was calculated in each period and the mean value of the four slopes was then considered as the index of baroreflex sensitivity (in ms/mm Hg) in each neonate. RESULTS: Spontaneous baroreflex sensitivity was lower in preterm neonates than in term neonates (mean(SD): 4.07 (2.19) ms/mm Hg vs 10.23 (2.92) ms/mm Hg). CONCLUSION: Baroreflex sensitivity can be assessed in term and preterm neonates by studying spontaneous variations in systolic blood pressure alone. This method could be useful for studying the ontogeny of baroreflex sensitivity and might therefore provide information about the maturation of the autonomic nervous system.

Baroreflex↗
PubMed2002

Development of baroreflex control of heart rate in preterm and full term infants.

AIM: To study baroreflex maturation by measuring, longitudinally, baroreflex sensitivity in preterm (gestational age 24-37 weeks) and full term infants. METHODS: Baroreflex sensitivity was quantified once a week, one to seven times, by a totally non-invasive method. RESULTS: Baroreflex sensitivity at birth was lower in the preterm infant and increased with gestational age. It also increased with postnatal age, but the values for the preterm infants at term still tended to be lower than the values for full term babies. CONCLUSION: Baroreflex control of heart rate is present in the premature infant, but is underdeveloped and increases with postnatal age. Ex utero maturation seems to be delayed compared with in utero maturation assessed by full term values. These results may reflect sympathovagal imbalance in preterm infants and could identify a population more vulnerable to stress.

Baroreflex↗
PubMed2002

Laboratory demonstration of baroreflex control of heart rate in conscious rats.

We have developed a laboratory exercise that demonstrates arterial baroreflex control of heart rate (HR) in the conscious unrestrained rat, incorporating graduate level physiological topics as well as a hands-on exposure to conscious animal research. This demonstration utilizes rats chronically instrumented to measure cardiac output (CO), HR, and arterial blood pressure in response to agents that raise or lower blood pressure. The HR response to progressive increases or decreases in blood pressure is recorded, and a baroreflex curve is generated by plotting mean arterial blood pressure (MABP) vs. HR. Observation of altered CO allows for discussion of the relationship between MAP, CO, HR, stroke volume, and total peripheral resistance. Administration of arginine vasopressin demonstrates the ability of this hormone to alter the sensitivity of the baroreflex. Throughout the demonstration, students answer questions from a handout about general cardiovascular physiology, specific pathways of agonists, and the baroreflex system, encouraging group and individual critical analysis of the results. Interpretation of the data reemphasizes lecture material and allows students to observe the baroreflex response in a physiological setting.

Animals↗
PubMed2003

Central command blunts the baroreflex bradycardia to aortic nerve stimulation at the onset of voluntary static exercise in cats.

To examine whether the central characteristics of the aortic baroreflex alter from moment to moment during static exercise, we identified the dynamic changes in the sizes of the bradycardia and depressor response evoked by stimulation of the aortic depressor nerve (ADN). Three conscious cats were trained to voluntarily extend the right forelimb and press a bar for 31 +/- 1 s with a peak force of 337 +/- 22 g while maintaining a sitting posture. The ADN stimulation-induced bradycardia was attenuated at the initial period of exercise (up to 8 s from the exercise onset) to 62 +/- 5% of the preexercise bradycardia and remained blunted until the end of exercise. The most blunted bradycardia was observed immediately before or when the forelimb was extended before force development. The baroreflex-induced bradycardia was suppressed again at cessation of exercise when the forelimb was retracted and recovered within a few seconds. In contrast, static exercise did not affect the ADN stimulation-induced depressor response. The ADN stimulation-induced bradycardia was also blunted at the beginning of naturally occurring body movement such as spontaneous postural change or grooming behavior. Thus it is likely that the central characteristics of the aortic baroreflex dynamically change from moment to moment during voluntary static exercise and during natural body movement and that particularly a central inhibition of the cardiac component of the aortic baroreflex is induced by central command at the onset of static exercise, whereas the central property of the vasomotor component of the baroreflex is preserved.

Animals↗
PubMed2002

alpha(2)-Adrenergic receptors in NTS facilitate baroreflex function in adult spontaneously hypertensive rats.

We examined the effect of alpha(2)-adrenoreceptor blockade in the nucleus of the solitary tract (NTS) on baroreflex responses elicited by electrical stimulation of the left aortic depressor nerve (ADN) in urethane-anesthetized spontaneously hypertensive rats (SHR, n = 11) and normotensive Wistar-Kyoto rats (WKY, n = 11). ADN stimulation produced a frequency-dependent decrease in mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate (HR). In SHR, unilateral microinjection of idazoxan into the NTS markedly reduced baroreflex control of MAP, RSNA, and HR and had a disproportionately greater influence on baroreflex control of MAP than of RSNA. In WKY, idazoxan microinjections did not significantly alter baroreflex function relative to control vehicle injections. These results suggest that baroreflex regulation of arterial pressure in SHR is highly dependent on NTS adrenergic mechanisms. The reflex regulation of sympathetic outflow to the kidney is less influenced by the altered alpha(2)-adrenoreceptor mechanisms in SHR.

Adrenergic alpha-Antagonists↗
PubMed2004

Influence of increased central venous pressure on baroreflex control of sympathetic activity in humans.

Volume expansion often ameliorates symptoms of orthostatic intolerance; however, the influence of this increased volume on integrated baroreflex control of vascular sympathetic activity is unknown. We tested whether acute increases in central venous pressure (CVP) diminished subsequent responsiveness of muscle sympathetic nerve activity (MSNA) to rapid changes in arterial pressure. We studied healthy humans under three separate conditions: control, acute 10 degrees head-down tilt (HDT), and saline infusion (SAL). In each condition, heart rate, arterial pressure, CVP, and peroneal MSNA were measured during 5 min of rest and then during rapid changes in arterial pressure induced by sequential boluses of nitroprusside and phenylephrine (modified Oxford technique). Sensitivities of integrated baroreflex control of MSNA and heart rate were assessed as the slopes of the linear portions of the MSNA-diastolic blood pressure and R-R interval-systolic pressure relations, respectively. CVP increased approximately 2 mmHg in both SAL and HDT conditions. Resting heart rate and mean arterial pressure were not different among trials. Sensitivity of baroreflex control of MSNA was decreased in both SAL and HDT condition, respectively: -3.1 +/- 0.6 and -3.3 +/- 1.0 versus -5.0 +/- 0.6 units.beat(-1).mmHg(-1) (P < 0.05 for SAL and HDT vs. control). Sensitivity of baroreflex control of the heart was not different among conditions. Our results indicate that small increases in CVP decrease the sensitivity of integrated baroreflex control of sympathetic nerve activity in healthy humans.

Adult↗