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PubMed1990

Cardiac baroreflex function during postural change assessed using non-invasive spontaneous sequence analysis in young men.

STUDY OBJECTIVE: The aim was to assess the value of baroreflex sensitivity estimates calculated from analyses of spontaneous systolic blood pressure and pulse interval sequences derived from continuous non-invasive finger blood pressure recordings during sitting and active standing. DESIGN: Continuous recordings of digital systolic blood pressure and pulse interval were obtained non-invasively using a Finapres FD5 during 5 min trials of sitting and standing. SUBJECTS: Subjects were healthy males aged 19-28, divided into those with "high" normal (n = 18) and "low" normal (n = 17) blood pressure. MEASUREMENTS AND MAIN RESULTS: Recordings were scanned for spontaneous sequences of three or more cardiac cycles over which systolic blood pressure increased progressively in conjunction with prolonged pulse interval, or decreased while pulse interval became shorter. Regressions between blood pressure and pulse interval (r greater than 0.80) provided estimates of cardiac baroreceptor reflex control. Computations were carried out with concurrent blood pressure and pulse interval measurements, and with a delay or lag of one and two cycles between the two variables. Pulse interval was reduced from an average 870.3 ms sitting to 571.3 ms on standing. Mean baroreflex sensitivity while sitting averaged 17.5 ms.mm Hg-1 at a delay of one cycle, failing to 7.65 ms.mm Hg-1 with standing. The decrease in sensitivity was correlated with the change in pulse interval between trials. The number of sequences was also significantly reduced with standing as opposed to sitting. Three cycle sequences were most frequent, with a lesser number of sequences involving 4, 5, and 6 or more cycles. No significant differences between "high" and "low" normal blood pressure groups were observed. CONCLUSIONS: The analysis of spontaneous sequences from non-invasive recordings may provide useful information concerning cardiac baroreflex control in different postural and behavioural states. A lag of one cycle between systolic blood pressure and pulse interval may provide the most representative estimates of baroreflex sensitivity.

Adult↗
PubMed1990

Differential effects of nitrous oxide on baroreflex control of heart rate and peripheral sympathetic nerve activity in humans.

Acute regulation of blood pressure in humans is mediated by arterial baroreflex regulation of heart rate, cardiac contractility, and peripheral sympathetic outflow. Brief pharmacologic reductions of blood pressure were employed in 11 healthy volunteers to determine the effects of N2O on baroreflex-mediated increases in heart rate and efferent muscle sympathetic nerve activity. R-R intervals (ECG), blood pressure (radial artery), central venous pressure, respiratory rate (abdominal bellows), and end-tidal gas concentrations (mass spectrometer) were monitored. Efferent sympathetic nerve activity directed to skeletal muscle blood vessels (MSNA) was recorded from an epoxy-coated tungsten needle placed into the peroneal nerve. Data were obtained from six subjects before and during iv bolus administration of sodium nitroprusside (100 micrograms), during control while breathing 40% N2/60% O2, during administration of N2O (40% N2O/60% O2), and during recovery (40% N2/60% O2). Five subjects served as time controls and breathed 40% N2 in O2 throughout the protocol. Nitrous oxide produced a 59 +/- 18% (P less than 0.05) increase in baseline MSNA but did not alter the reflex augmentations in MSNA produced by nitroprusside. In contrast, there was a 39 +/- 14% decrease in the slope of the relationship between systolic pressure and R-R interval (P less than 0.05) in subjects breathing N2O. N2O thus produces activation of the sympathetic nerves directed to skeletal muscle blood vessels, and it decreases baroreflex-mediated tachycardia without diminishing baroreflex-mediated augmentations in sympathetic outflow.

Adult↗
PubMed1988

Impaired baroreflex changes in muscle sympathetic nerve activity in adolescents who have a family history of essential hypertension.

To evaluate the baroreflex changes and basal sympathetic vasomotor tone among three groups of adolescent normotensives or borderline hypertensives with and normotensives without a family history of hypertension, we continuously recorded muscle sympathetic nerve activity, arterial pressure and heart interval. Baroreflex slopes were calculated either by plotting the heart interval against the preceding peak systolic arterial pressure, or by relating the percentage changes in muscle sympathetic nerve activity to the mean changes in systolic arterial pressure produced by intravenous phenylephrine. The baroreflex slopes for the heart interval were significantly smaller in borderline hypertensive offspring (14 +/- 2 ms/mmHg) than in control normotensives (23 +/- 2 ms/mmHg) or normotensive offspring (19 +/- 3 ms/mmHg), whereas those for muscle sympathetic nerve activity were significantly smaller both in normotensive offspring (-8.3 +/- 1.0%/mmHg) and borderline hypertensive offspring (-7.9 +/- 0.5%/mmHg) than in control normotensives (-16.3 +/- 1.4%/mmHg). Baseline muscle sympathetic nerve activity was higher in borderline hypertensive offspring (20.1 +/- 3.0 bursts/min) than in control normotensives (10.1 +/- 1.2 bursts/min) or normotensive offspring (12.8 +/- 1.4 bursts/min), and also the depressor responses to trimethaphan were significantly enhanced in borderline hypertensive offspring [-19.2 +/- 2 versus 14 +/- 1 (normotensive offspring) or 12 +/- 2 (control normotensives)]. These results indicate that baroreflex inhibition of muscle sympathetic nerve activity was reduced in adolescents with a family history of hypertension even when they were normotensive. This reduced reflex sympatho-inhibition could lead to the development of hypertension by increasing sympathetic vasomotor tone.

Adult↗
PubMed1993

Central effects of endothelin on baroreflex of spontaneously hypertensive rats.

OBJECTIVE: To study the contribution made by central endothelin to cardiovascular regulation in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) controls. METHODS: Central endothelin binding was measured with receptor autoradiography. The baroreceptor heart rate reflex was measured by sigmoidal curve-fitting of the mean arterial pressure and heart rate responses evoked by alternating intravenous injections of nitroprusside or phenylephrine. The baroreflex gain was derived as a function of the heart rate range and the curvature coefficient. RESULTS: Autoradiographic experiments with [125I]-endothelin-1 showed low to moderate binding in various medullary nuclei involved in cardiovascular regulation, such as the nucleus tractus solitarius and the ventrolateral medulla. A moderate binding density was found in regions such as the hypoglossal nucleus and the spinal trigeminal nucleus, whereas a high binding density was observed in the molecular layer of the cerebellum. The binding density was significantly lower in the ventrolateral medulla of SHR than in that of WKY rats, but there were no differences in other medullary regions. Compared with WKY rats, the SHR had higher mean arterial pressures and heart rates but tended to have a reduced baroreceptor heart rate reflex gain. This latter change was entirely attributed to a significantly lower heart rate range, caused by an elevated lower heart rate plateau in SHR. The intracisternal injection of endothelin-1 at 25 pmol/kg did not influence the resting mean arterial pressure or heart rate, but it caused a significant increase in baroreflex gain, in both SHR and WKY rats. The extent of the effect was similar in the two strains and was attributed to a significant increase in the curvature coefficient of the sigmoidal baroreflex curve. Consequently, the range over which blood pressure changes evoked reflex changes in the heart rate was reduced by endothelin-1 treatment in both SHR and WKY rats. The heart rate range was not affected and remained different between SHR and WKY rats after the endothelin-1 injection. The intracisternal injection of endothelin-3 at 25 pmol/kg, but not at 2.5 pmol/kg, had effects similar to those of endothelin-1 on the baroreflex. CONCLUSIONS: These results show that binding sites for endothelin-1 are present in various regions of the hindbrain of SHR and WKY rats and that central administration of endothelin-1 sensitizes the baroreceptor heart rate reflex. However, this latter effect is similar in SHR and WKY rats and is mediated by a mechanism which is distinct from that underlying the difference in reflex sensitivity between these strains.

Animals↗
PubMed1996

Relationship between mechanical properties of the carotid artery wall and baroreflex function in acutely treated hypertensive patients.

OBJECTIVE: To evaluate the relationship between the mechanical properties of the carotid artery wall and baroreflex function after acute reduction of blood pressure with lacidipine in essential hypertension. DESIGN: After 15 days of placebo washout, the hypertensive patients underwent a single-blind haemodynamic study before and 90 min after administration of 4 mg lacidipine (a dihydropyridine calcium antagonist). METHODS: Brachial intra-arterial blood pressure was recorded in eight mild-to-moderate essential hypertensive patients aged 40-53 years (mean +/- SEM 46.8 +/- 4.7 years). The carotid pulse diameter was recorded simultaneously by an echo-tracking technique. The mechanical properties of the carotid artery wall were evaluated by calculating Peterson's incremental elastic modulus (Ep) both as an averaged value of 10 heart cycles with stable blood pressure and was the dynamic correlation, on a beat-to-beat basis, of Ep and the systolic blood pressure during a 20 mmHg increase in blood pressure following a bolus injection of phenylephrine. The elastic properties of the carotid artery were investigated further by determining the correlation between the systolic pressure and systolic diameter, beat by beat, during a ramped increase of blood pressure after phenylephrine administration. The baroreceptor reflex sensitivity was measured simultaneously by the Oxford method and by correlating Ep and the electrocardiographic R-R' interval on a beat-to-beat basis during phenylephrine injections. RESULTS: After lacidipine administration Peterson's elastic modulus, measured under resting steady-state conditions, was reduced (18.7 +/- 7.4 versus 16.4 +/- 6 x 10(5) dyne/cm2), whereas the baroreflex sensitivity was unchanged (6.6 +/- 3.3 versus 6.3 +/- 0.2 ms/mmHg) and resetting of the baroreflex had occurred. At the same time, the correlations between the systolic blood pressure and Ep and between the systolic blood pressure and carotid systolic diameter over a 20 mmHg increase in blood pressure were unchanged. Moreover, the correlations between the systolic blood pressure and the R-R' interval and between Ep and R-R' interval during the phenylephrine-induced blood pressure increase did not differ statistically. CONCLUSIONS: The results suggest that the resetting of the baroreflex after the acute reduction in blood pressure caused by lacidipine is dissociated from mechanical changes in the carotid artery wall.

Adult↗
PubMed1991

Baroreflex and atrial natriuretic factor concentration correlate with myocardial infarct size and predict early death in rabbits: implications for drug studies.

The severity of myocardial infarction (MI) and its functional consequences are difficult to assess in small animals. We searched for criteria to achieve such an assessment in rabbits 1 week after MI. Thirteen large mongrel rabbits (3-4 kg) were anesthetized with pentobarbitone for ligating a branch of the circumflex coronary artery and 7 rabbits were subject to a sham operation without ligation. All sham-operated rabbits and 12 MI animals survived for 1 week, when blood was obtained for biochemical analyses and the baroreflex was tested. Six animals survived to the third week (survivors) and six died earlier (nonsurvivors). The MI size, measured immediately after death, was 42 +/- 3% of the left ventricular mass in nonsurvivors and 20 +/- 7% in survivors. The plasma atrial natriuretic factor (ANF) concentration was correlated linearly with MI size (r = 0.77) over the whole range of infarct sizes and, like the MI size itself, was associated with the risk of early death (critical limit: 80 pM). Plasma renin activity and catecholamines yielded less prognostic information. The baroreflex control of the heart rate (tested using phenylephrine and nitroprusside) of nonsurvivors was severely impaired and the slopes correlated with MI size (r = 0.90 for phenylephrine and r = 0.67 for nitroprusside). The plasma ANF concentration and the baroreflex both accurately reflected MI size and also correctly classified 11/12 rabbits into survivors and nonsurvivors. An ANF- and baroreflex-based stratification of animals for future studies on therapeutic interventions after MI will reduce the number of animals required by at least 65%, making such studies far more feasible than in the past.

Animals↗
PubMed1992

Baroreflex control of heart rate during high thoracic epidural anaesthesia. A randomised clinical trial on anaesthetised humans.

Baroreflex control of heart rate after cardiac sympathectomy induced by thoracic epidural anaesthesia was evaluated in 30 patients who were randomly assigned to group 1 (bupivacaine 0.25%), group 2 (bupivacaine 0.5%) or group 3 (control). Plasma volume expanders were given to equalize preload conditions, as assessed using transoesophageal echocardiography. All measurements were made under general anaesthesia. Baroreflex sensitivity was determined from the heart rate response to phenylephrine and nitroglycerin. There was no difference in cardiac slowing in response to phenylephrine between the three groups. Baroreflex sensitivity, measured as cardiac acceleration in response to nitroglycerin, was significantly lower (p < 0.01) in groups 1 and 2 (1.8 and 1.5 ms.mmHg-1 respectively) compared with group 3 (3.5 ms.mmHg-1) with no differences between the two bupivacaine concentrations. The results suggest that baroreflex-mediated response to decreases in arterial pressure is dependent on the integrity of the sympathetic nervous system.

Adult↗
PubMedDate not supplied

Angiotensin and the cardiac baroreflex response to phenylephrine.

1. In adult conscious sheep the pressor actions of infused angiotensin II were prevented by the concomitant intravenous infusions of sodium nitroprusside. The effect of such intravenous infusions of angiotensin II on the cardiac baroreflex response to transient rises in arterial pressure caused by intravenous phenylephrine was studied. 2. Intravenous infusion of angiotensin II caused a reduction in pulse interval in the absence of any change in arterial pressure. It also caused a reduction in baroreflex sensitivity measured by determining the relation between pulse interval and systolic pressure during the rise in pressure caused by injection of phenylephrine. 3. After administration of the converting enzyme inhibitor (captopril) the mean baroreflex sensitivity of 3 of 4 pregnant ewes increased. 4. It is concluded that high levels of angiotensin II can modify the cardiac baroreceptor reflex response so that the heart rate is inappropriately high for a given systolic pressure and that it reduces the sensitivity of the cardiac baroreflex response to transient changes in arterial pressure.

Angiotensin II↗
PubMed1989

Evolution with age of baroreflex sensitivity and its autonomic nervous components in conscious hypertensive rats of the Lyon strain.

1. Cardiac baroreflex sensitivity (BRS) and its sympathetic and vagal components were studied after atropine and propranolol administrations in conscious genetically hypertensive (LH), normotensive (LN) and low blood pressure (LL) rats of the Lyon strain at 5, 9, 13 and 70 weeks of age. 2. LH rats older than 9 weeks exhibit a lower BRS than age-matched LN and LL controls. 3. The vagal component of cardiac baroreflex is predominant. In LN rats, this component increases up to 9 weeks of age. 4. The sympathetic component of cardiac baroreflex is small and identical in the three strains and does not alter with age. 5. Thus, in normotensive rats, the increase in BRS during maturation reflects mainly the vagal component. The development of hypertension prevents this physiological increase in the sensitivity of the vagal component of cardiac baroreflex leading to a reduced BRS.

Aging↗
PubMed1993

Changes in plasma volume and baroreflex function following resistance exercise.

The dynamics of change in plasma volume (PV) and baroreflex responses have been reported over 24 h immediately following maximal cycle exercise. The purpose of this study was to determine if PV and baroreflex showed similar changes for 24 h after resistance exercise. Eight men were studied on 2 test days, 1 week apart. On 1 day, per cent change (% delta) in PV was estimated at 0,3, and 6 h after resistance exercise using haematocrit and haemoglobin. Baseline PV was measured 24 h after exercise using Evans blue dye. The carotid baroreceptor-cardiac reflex response was measured before, and 3, 6, 9, 12, and 24 h post-exercise. Each subject performed six sets of the bench press and leg press with 10 repetitions per set with a load that induced failure within each set. On a control day, the protocol was used without exercise. Plasma volume did not change during the control day. There was a 20% decrease in PV immediately post-exercise; the recovery of the PV was rapid and complete within 3 h. PV was 20% greater 24 h post-exercise than on the control day. There were no differences in any of the baroreflex measurements. Therefore, it is suggested that PV shifts may occur without altering baroreflex sensitivity.

Adult↗
PubMed1980

Phase relationship between normal human respiration and baroreflex responsiveness.

1. We studied the influences of phase of respiration and breathing frequency upon human sinus node responses to arterial baroreceptor stimulation. 2. Carotid baroreceptors were stimulated with brief (0.6 sec), moderate (30 mmHg) neck suction during early, mid, and late inspiration or expiratin at usual breathing rates, or, during early inspiration and expiration at breathing rates of 3, 6, 12, and 24 breaths/min. 3. Baroreceptor stimuli applied during early and mid inspiration and late expiration provoked only minor sinus node inhibition; stimuli begun during late inspiration and early expiration provoked maximum sinus node inhibition. 4. At breathing rates of 3, 6 and 12 breaths/min, expiratory baroreflex responses were significantly greater than inspiratory responses; at 24 breaths/min, however, inspiratory and expiratory baroreceptor stimuli produced comparable degrees of sinus node inhibition. 5. Our results delineate an important central biological rhythm in normal man: human baroreflex responsiveness oscillates continuously during normal, quiet respiration. The phase shift of baroreflex responsiveness on respiration suggests that this interaction cannot be ascribed simply to gating synchronous with central inspiratory neurone activity. Regularization of heart rate during rapid breathing is associated with loss of the differential inspiratory-expiratory baroreflex responsiveness which is present at usual breathing rates.

Adult↗
PubMed1976

Baroreflex sensitivity and responses to the Valsalva manoeuvre in subjects with diabetes mellitus.

Baroreflex sensitivity was measured in a group of diabetic patients from the slope of the regression of pulse interval on systolic arterial pressure, during elevation of pressure induced by phenylephrine. The response to Valsalva's manoeuvre was assessed in the same subjects. There was a good correlation between the two tests in the identification of patients with a parasympathetic autonomic disturbance, but measurements of baroreflex sensitivity were more readily quantifiable than were the responses to Valsalva's manoeuvre. Furthermore, baroreflex sensitivity could be measured in patients with sympathetic nervous dysfunction in whom vagal function could not be assessed by means of the Valsalva manoeuvre. Measurement of baroreflex sensitivity is likely to be suitable for longitudinal studies of the progress of diabetic autonomic neuropathy.

Adult↗
PubMed1982

Baroreflex regulation of renal nerve activity during volume expansion.

Volume expansion could inhibit renal nerve activity by stimulating cardiopulmonary baroreflexes or by increasing arterial pressure (i.e., stimulating the sinoaortic baroreflexes). Our study assessed the relative roles of these two reflexes in the renal nerve activity responses to volume expansion (15 ml/kg 6% dextran in normal saline). With cardiopulmonary and arterial baroreflexes intact, volume expansion resulted in increases in arterial pressure and pulmonary artery wedge pressure and in decreases in renal nerve activity. After sinoaortic denervation, volume expansion resulted in similar decreases in renal nerve activity for similar increases in pulmonary artery wedge pressure. In contrast, after selective vagotomy (sinoaortic baroreflexes intact) volume expansion resulted in increases in arterial pressure and pulmonary artery wedge pressure, but reductions in renal nerve activity were markedly attenuated. After sinoaortic denervation and vagotomy, volume expansion did not result in significant changes in renal nerve activity. We conclude that decreases in renal nerve activity during volume expansion are mediated mainly by cardiopulmonary receptors with afferent vagal fibers. Sinoaortic baroreceptors appear to play a minor role in mediating these responses.

Animals↗
PubMed1986

Sites at which vasopressin facilitates baroreflex inhibition of lumbar sympathetic nerve activity.

We recently reported that intravenous vasopressin in anesthetized rabbits facilitates baroreflex inhibition of lumbar sympathetic nerve activity. The purpose of this study was to determine the possible sites of this facilitation. We found that intravenous infusion of vasopressin (16-32 mU X kg-1 X min-1) caused greater inhibition of lumbar sympathetic nerve activity than did phenylephrine for a given increase in aortic baroreceptor activity, suggesting a "central" action of vasopressin. A central action was supported also by the observation that the carotid baroreflex inhibition of lumbar sympathetic nerve activity was augmented by intravenous infusion of vasopressin when the carotid sinuses were isolated, filled with saline, and distended (aortic depressor and vagal nerves were cut). On the other hand, vasopressin also facilitated baroreflex inhibition of lumbar sympathetic nerve activity through an influence on arterial baroreceptors, because intravenous vasopressin caused greater afferent activity of the aortic depressor nerve per unit rise in arterial pressure than did phenylephrine. In a separate group of rabbits, intravenous infusion of vasopressin also elevated the level of afferent aortic depressor activity during increases in arterial pressure induced by intra-aortic balloon inflation. Furthermore, when vasopressin was confined to the isolated carotid sinuses, the reflex inhibition of lumbar sympathetic nerve activity during distension of carotid sinuses was augmented. We conclude that circulating vasopressin facilitates baroreflex inhibition of sympathetic nerve activity through a central nervous system action as well as through an effect on arterial baroreceptors.

Administration, Topical↗
PubMed1986

Blood pressure and baroreflex sensitivity in conscious hypertensive rats of Lyon strain.

The evolution with age of blood pressure (BP), heart rate (HR), and baroreflex sensitivity was studied in hypertensive (LH), normotensive (LN), and low blood pressure (LL) male rats of the Lyon strains. Intra-arterial BP was continuously recorded for 48 h in freely moving animals. On-line computer analysis of the BP curve allowed calculation of systolic (SBP), mean (MAP), and diastolic (DBP) blood pressure, HR, and their variability. At 5 wk of age, LH rats exhibited a higher BP than LN and LL controls, which, at 21 wk of age, was associated with significant bradycardia and a greater variability in DBP and HR. LL rats had a MAP similar to LN, which confirms that both strains are, in terms of BP, valid controls for LH animals. The baroreflex sensitivity measured after phenylephrine injections increased with age more markedly in LN and LL than in LH rats, whereas in the latter, it was significantly lower at the age of 9 and 21 wk. When measured after nitroglycerin injections, the baroreflex sensitivity was higher and more stable than that observed after phenylephrine administration. In addition, the baroreflex sensitivity in the different strains was inversely related to the level and the variability of DBP but not of HR.

Aging↗
PubMed1990

Neurons in area postrema mediate vasopressin-induced enhancement of the baroreflex.

Intravenous infusion of arginine vasopressin (AVP) has been shown to enhance baroreflex sensitivity, and this enhancement is dependent on the integrity of the area postrema. However, previous studies did not differentiate a role for cell bodies in the area postrema vs. the dense network of fibers located in and around the lateral and ventral margins of this circumventricular organ. In the present study, baroreflex function was assessed in conscious rabbits by examining heart rate after ramp infusions of phenylephrine (PE) and AVP. The subsequent day, the excitotoxin kainic acid was injected (30 nl initially, with five 15-nl supplemental injections of a 1 ng/nl solution over 1 h) into the area postrema, thus selectively destroying cell bodies. After an 8-day recovery period, baroreflex function was again assessed. The bradycardic response to graded infusion of PE (slope = -2.29 +/- 0.30) was not significantly different after selective lesions of area postrema neurons (slope = -1.88 +/- 0.49). In contrast, the previously enhanced bradycardic response to infusion of AVP (slope = -5.76 +/- 1.02) was significantly attenuated (slope = -2.31 +/- 0.21) to levels similar to that seen with infusion of PE. Thus selective chemical lesions of area postrema neurons block vasopressin-induced enhancement of the baroreflex.

Animals↗
PubMed1991

Increase in sympathetic activity with age. I. Role of impairment of arterial baroreflexes.

The purpose of this study was to evaluate changes in arterial baroreflex function with aging. Mean arterial pressure (MAP) obtained in the awake state was 110 +/- 7 mmHg in the young animals (1 yr; n = 5) and 128 +/- 6 mmHg in the old beagles (11 yr; n = 11) (P less than 0.05). In response to bolus administration of varying doses of phenylephrine and nitroglycerin in the conscious state, the slope relating heart rate (HR) to MAP was attenuated significantly in the old animals compared with the young (-0.87 +/- 0.30 vs. -2.35 +/- 0.44 beats.min-1.mmHg-1; P less than 0.05). After atropine, the baroreflex control of HR was abolished in both groups. After anesthesia and sectioning of the aortic depressor nerves, and with isolated carotid sinus pressures (CSP) held at 50 mmHg, absolute renal sympathetic nerve activity (RSNA) was significantly greater in the old (368 +/- 40 Hz) vs. the young animals (41 +/- 9 Hz). In the old, the gains of baroreflex inhibition of MAP (0.78 +/- 0.09) and normalized RSNA (0.38 +/- 0.14%/mmHg) during increases in CSP were decreased significantly compared with the young (MAP, 1.16 +/- 0.17 mmHg, and RSNA, 0.72 +/- 0.06%/mmHg). In a subgroup of old normotensive animals (n = 5), the baroreflex gain of RSNA was still attenuated (0.43 +/- 0.11%/mmHg) compared with the young. The reflex reduction in absolute RSNA as a function of baseline RSNA was also impaired in old vs. young beagles.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1992

Is there a central nervous system component to acute baroreflex resetting in rats?

This study was designed to evaluate a possible central nervous system (CNS) component to acute baroreflex resetting. In nine arterial baroreceptor-denervated, chloralose-urethan-anesthetized rats, a control (C) aortic nerve stimulation curve (3-5 V, 1 ms, 0-64 Hz) was obtained. Next, a constant "baroreceptor" input was delivered to the CNS (left aortic nerve stimulation, 10 min, 10.2 +/- 1.5 Hz). Within the first 13 s of aortic nerve stimulation, maximum inhibition of lumbar sympathetic nerve activity (LSNA) was 60 +/- 7.8% of baseline and at 1 min it increased to 68 +/- 5.6% of baseline. At the end of the 10-min aortic nerve stimulation, LSNA was not different from the response at 1 min (68 +/- 5.6% = 74 +/- 4.1%). Immediately after the constant stimulation (within 30 s), a test or reset (RS) curve was obtained (0-64 Hz). A recovery (RC) curve was obtained 10-20 min later. The slope of the linear portion of the curve and the stimulation frequency that produced 50% maximum inhibition (ES50) were compared among the three baroreflex curves (C, RS, RC,) and no significant differences were found. Thus, although a CNS component to baroreflex adaptation was evident during the first minute of aortic nerve stimulation, a longer term acute resetting of the baroreflex curve did not occur.

Animals↗