Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Baroreflex”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed1995

Facilitation of the arterial baroreflex by the preoptic area in anaesthetized rats.

1. Activation of cell bodies in the ventrolateral part of the midbrain periaqueductal grey matter (PAG) facilitates the arterial baroreflex via the nucleus raphe magnus. The facilitatory effects of stimulation within the hypothalamus on the arterial baroreflex and their relation to the PAG and nucleus raphe magnus were studied in urethane- and chloralose-anaesthetized rats. 2. Systematic mapping experiments revealed that the preoptic area (POA) is the principal location in the hypothalamus of neuronal cell bodies that are responsible for the potentiation of the baroreflex. In addition to provoking hypotension and vagal bradycardia, both electrical and chemical stimulation of the POA produced facilitation of baroreflex vagal bradycardia (BVB) that was evoked by electrical stimulation of the aortic depressor nerve. Baroreflex hypotension was slightly augmented during activation of the POA in vagotomized rats. 3. Selective destruction of cell bodies either in the ventrolateral PAG or in the nucleus raphe magnus reduced facilitation of BVB by the POA. Hypotension and bradycardia due to POA stimulation were also markedly attenuated after such selective destruction. 4. In conclusion, the POA, the ventrolateral PAG and the nucleus raphe magnus constitute a functional complex that produces cardiovascular trophotropic effects including hypotension, vagal bradycardia and baroreflex facilitation.

Anesthesia↗
PubMed2003

Peripheral chemoreflex and baroreflex interactions in cardiovascular regulation in humans.

We tested the hypothesis that activation of peripheral chemoreceptors with acute isocapnic hypoxia resets arterial baroreflex control of both heart rate and sympathetic vasoconstrictor outflow to higher pressures, resulting in increased heart rate and muscle sympathetic nerve activity without changes in baroreflex sensitivity. We further hypothesized that this resetting would not occur during isocapnic hyperpnoea at the same breathing rate and depth as during isocapnic hypoxia. In 12 healthy, non-smoking, normotensive subjects (6 women, 6 men, 19-36 years), we assessed baroreflex control of heart rate and muscle sympathetic nerve activity using the modified Oxford technique during normoxia, isocapnic hyperpnoea, and isocapnic hypoxia (85 % arterial O2 saturation). While isocapnic hyperpnoea did not alter heart rate, arterial pressure, or sympathetic outflow, hypoxia increased heart rate from 61.9 +/- 1.8 to 74.7 +/- 2.7 beats min-1 (P < 0.05), increased mean arterial pressure from 97.4 +/- 2.0 to 103.9 +/- 3.3 mmHg (P < 0.05), and increased sympathetic activity 22 +/- 13 % relative to normoxia and 72 +/- 21 % (P < 0.05) relative to hyperpnoea alone. The sensitivity for baroreflex control of both heart rate and sympathetic activity was not altered by either hypoxia or hyperpnoea. Thus, it appears that acute activation of peripheral chemoreceptors with isocapnic hypoxia resets baroreflex control of both heart rate and sympathetic activity to higher pressures without changes in baroreflex sensitivity. Furthermore, these effects appear largely independent of breathing rate and tidal volume.

Adult↗
PubMed2005

Resetting of the arterial baroreflex increases orthostatic sympathetic activation and prevents postural hypotension in rabbits.

Since humans are under ceaseless orthostatic stress, the mechanism to maintain arterial pressure (AP) under orthostatic stress against gravitational fluid shift is of great importance. We hypothesized that (1) orthostatic stress resets the arterial baroreflex control of sympathetic nerve activity (SNA) to a higher SNA, and (2) resetting of the arterial baroreflex contributes to preventing postural hypotension. Renal SNA and AP were recorded in eight anaesthetized, vagotomized and aortic-denervated rabbits. Isolated intracarotid sinus pressure (CSP) was increased stepwise from 40 to 160 mmHg with increments of 20 mmHg (60 s for each CSP level) while the animal was placed supine and at 60 deg upright tilt. Upright tilt shifted the CSP-SNA relationship (the baroreflex neural arc) to a higher SNA, shifted the SNA-AP relationship (the baroreflex peripheral arc) to a lower AP, and consequently moved the operating point to marked high SNA while maintaining AP. A simulation study suggests that resetting in the neural arc would double the orthostatic activation of SNA and increase the operating AP in upright tilt by 10 mmHg, compared with the absence of resetting. In addition, upright tilt did not change the CSP-AP relationship (the baroreflex total arc). A simulation study suggests that although a downward shift of the peripheral arc could shift the total arc downward, resetting in the neural arc would compensate this fall and prevent the total arc from shifting downward to a lower AP. In conclusion, upright tilt increases SNA by resetting the baroreflex neural arc. This resetting may compensate for the reduced pressor responses to SNA in the peripheral cardiovascular system and contribute to preventing postural hypotension.

Adaptation, Physiological↗
PubMed2006

Effect of repetitive hypoxic apnoeas on baroreflex function in humans.

Baroreflex function is impaired in patients with obstructive sleep apnoea. We tested the hypothesis that short-term exposure to repetitive hypoxic apnoeas (RHA) produces prolonged impairment in baroreflex function. Baroreflex function was determined using the modified Oxford technique in 14 subjects (26 +/- 1 years). Baroreflex sensitivity (BRS) was quantified from the R-R interval-systolic blood pressure (BP; cardiovagal BRS), heart rate-systolic BP (HR BRS) and muscle sympathetic nerve activity (MSNA)-diastolic BP (sympathetic BRS) relations. RHA involved subjects performing repetitive end-expiratory apnoeas (20 s) every minute for 30 min during intermittent hypoxia to accentuate oxygen desaturation. After RHA, BP and MSNA at rest were elevated. BRS was measured approximately 7 (Post 1), approximately 30 (Post 2) and approximately 50 min (Post 3) after RHA to provide insight into the temporal pattern of responses. Cardiovagal BRS (16.8 +/- 1.3, 16.5 +/- 1.6, 17.6 +/- 2.0 and 17.4 +/- 1.5 ms mmHg(-1) for Pre, Post 1, Post 2 and Post 3, respectively), HR BRS (-1.1 +/- 0.1, -1.1 +/- 0.1, -1.3 +/- 0.1 and -1.4 +/- 0.1 beats min(-1) mmHg(-1)) and sympathetic BRS (-4.5 +/- 0.6, -4.4 +/- 0.7, -3.7 +/- 0.5 and -4.7 +/- 1.0 arbitrary units (au) beat(-1) mmHg(-1)) were unchanged by RHA. In contrast, the operating points of the baroreflexes were shifted rightward (to higher levels of BP) and upward (to higher levels of heart rate and MSNA) after RHA (P < 0.05). Time control studies performed in five additional subjects showed no change in any of the measured variables over time. Collectively, these data indicate that short-term exposure to RHA shifts ('resets') the baroreflex stimulus-response curve to higher levels of BP without influencing BRS for extended periods of time.

Adolescent↗
PubMed2002

Cyclosporine adversely affects baroreflexes via inhibition of testosterone modulation of cardiac vagal control.

Previous studies have shown that the immunosuppressant drug cyclosporine A attenuates arterial baroreceptor function. This study investigated whether the modulatory effect of cyclosporine on baroreceptor function involves inhibition of the baroreflex-facilitatory effect of testosterone. The role of cardiac autonomic control in cyclosporine-testosterone baroreflex interaction was also investigated. Baroreflex curves relating bradycardic responses to increments in blood pressure evoked by phenylephrine were constructed in conscious, sham-operated, castrated rats and in testosterone-replaced castrated (CAS + T) rats in the absence and presence of cyclosporine. The slopes of the curves were taken as an index of the baroreflex sensitivity (BRS). Short-term (11-13 days) cyclosporine treatment or castration reduced plasma testosterone levels and caused similar attenuation of the reflex bradycardia, as indicated by the significantly smaller BRS compared with sham-operated values (-0.97 +/- 0.07, -0.86 +/- 0.06, and -1.47 +/- 0.10 beats/min/mm Hg, respectively). The notion that androgens facilitate baroreflexes is further confirmed by the observation that testosterone replacement of castrated rats restored plasma testosterone and BRS to sham-operated levels. Cyclosporine had no effect on BRS in castrated rats but caused a significant reduction in CAS + T rats. Muscarinic blockade by atropine caused approximately 60% reduction in the BRS in sham-operated rats, an effect that was significantly and similarly diminished by castration, cyclosporine, or their combination. beta-Adrenergic blockade by propranolol caused no significant changes in BRS. These findings suggest that cyclosporine attenuates baroreflex responsiveness via, at least partly, inhibition of the testosterone-induced facilitation of cardiomotor vagal control.

Adrenergic alpha-Agonists↗
PubMed1995

Baroreflex sensitivity and cardiovascular mortality in patients with mild to moderate heart failure.

OBJECTIVE: To assess the influence of both sympathetic (plasma noradrenaline concentrations) and parasympathetic (baroreflex activation) tone on survival in patients with congestive heart failure. DESIGN: Invasive study with determination of parasympathetic activity and follow up for at least 4.5 years. SUBJECTS: 35 patients with sinus rhythm and mild to moderate heart failure (New York Heart Association grades II-III) (mean age 53 (SD 3)). RESULTS: 20 patients whose hearts survived were compared with 15 patients whose hearts did not (12 died and three received transplants). The two groups differed significantly in terms of mean arterial blood pressure (98 (3) v 90 (3) mm Hg), heart rate (82 (2) v 93 (4) beats/min), and mean pulmonary artery pressure (24 (3) v 35 (2) mm Hg) (all P < 0.05), while cardiac index, stroke volume index, and right atrial pressures were not different. The survivors had significantly lower plasma renin activities (3.6 (0.8) v 9.0 (3.6) angiotensin I/ml/h; P < 0.05) and tended to have lower noradrenaline values than non-survivors (170 (23) v 286 (74) pg/ml) at baseline. Baroreflex sensitivity was significantly lower in non- survivors than in survivors (1.3 (0.2) v 2.3 (0.3) ms/mm/Hg); P < 0.02). As the time of cardiac transplantation is dependent on complex logistical factors the three patients who received a transplant were excluded from the analysis of survival time. The risk of death in relation to baroreflex sensitivity at the median sensitivity of 1.48 ms/mm Hg was calculated. Survival was significantly different (P < 0.04) between the resulting two groups; three of the 16 subjects with high baroreflex sensitivity died compared with nine of the 16 with a baroreflex sensitivity < 1.48 ms/mm Hg. When systemic blood pressure, pulmonary artery pressure, stroke volume index, plasma noradrenaline concentrations, and baroreflex sensitivity were entered into a Cox proportional hazards regression, only systolic blood pressure and plasma noradrenaline values predicted survival (P < 0.001). CONCLUSIONS: Low vagal tone is correlated with a poor prognosis in patients with heart failure. Sympathetic tone measured as plasma noradrenaline concentration also contributed to survival. An additional contribution of vagal tone to survival could not be shown when sympathetic tone was considered simultaneously. This may be due to the inverse relation of sympathetic and parasympathetic tone and to the insensitivity of the multiple regression method to identify additional risk factors in small numbers of patients.

Baroreflex↗
PubMed2003

nNOS gene transfer to RVLM improves baroreflex function in rats with chronic heart failure.

We hypothesized that gene transfer of neuronal nitric oxide synthase (nNOS) into the rostral ventrolateral medulla (RVLM) improves baroreflex function in rats with chronic heart failure (CHF). Six to eight weeks after coronary artery ligation, rats showed hemodynamic signs of CHF. A recombinant adenovirus, either Ad.nNOS or Ad.beta-Gal, was transfected into the RVLM. nNOS expression in the RVLM was confirmed by Western blot analysis, NADPH-diaphorase, and immunohistochemical staining. We studied baroreflex control of the heart rate (HR) and renal sympathetic nerve activity (RSNA) in the anesthetized state 3 days after gene transfer by intravenous injections of phenylephrine and nitroprusside. Baroreflex sensitivity was depressed for HR and RSNA regulation in CHF rats (2.0 +/- 0.3 vs. 0.8 +/- 0.2 beats.min-1.mmHg-1, P < 0.01 and 3.8 +/- 0.3 vs. 1.2 +/- 0.1% max/mmHg, P < 0.01, respectively). Ad.nNOS transfer into RVLM significantly increased the HR and RSNA ranges (152 +/- 19 vs. 94 +/- 12 beats/min, P < 0.05 and 130 +/- 16 vs. 106 +/- 5% max/mmHg, P < 0.05) compared with the Ad.beta-Gal in CHF rats. Ad.nNOS also improved the baroreflex gain for the control of HR and RSNA (1.8 +/- 0.2 vs. 0.8 +/- 0.2 beats.min-1.mmHg-1, P < 0.01 and 2.6 +/- 0.2 vs. 1.2 +/- 0.1% max/mmHg, P < 0.01). In sham-operated rats, we found that Ad.nNOS transfer enhanced the HR range compared with Ad.beta-Gal gene transfer (188 +/- 15 vs. 127 +/- 14 beats/min, P < 0.05) but did not alter any other parameter. This study represents the first demonstration of altered baroreflex function following increases in central nNOS in the CHF state. We conclude that delivery of Ad.nNOS into the RVLM improves baroreflex function in rats with CHF.

Animals↗
PubMed2002

Role of the area postrema in angiotensin II modulation of baroreflex control of heart rate in conscious mice.

This study reports the effects of angiotensin II (ANG II), arginine vasopression (AVP), phenylephrine (PE), and sodium nitroprusside (SNP) on baroreflex control of heart rate in the presence and absence of the area postrema (AP) in conscious mice. In intact, sham-lesioned mice, baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of ANG II were significantly less than those observed with similar increases in arterial pressure with PE (slope: -3.0 +/- 0.9 vs. -8.1 +/- 1.5 beats x min(-1) x mmHg(-1)). Baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of AVP were the same as those observed with PE in sham animals (slope: -5.8 +/- 0.7 vs. -8.1 +/- 1.5 beats x min(-1) x mmHg(-1)). After the AP was lesioned, the slope of baroreflex inhibition of heart rate was the same whether pressure was increased with ANG II, AVP, or PE. The slope of the baroreflex-induced increases in heart rate due to decreases in arterial blood pressure with SNP were the same in sham- and AP-lesioned animals. These results indicate that, similar to other species, in mice the ability of ANG II to acutely reset baroreflex control of heart rate is dependent on an intact AP.

Angiotensin II↗
PubMed1994

Relation between baroreflex sensitivity and cardiac vagal tone in humans.

The extent of dependence of cardiac vagal tone on arterial baroreceptor input has been studied in 12 healthy, young adult subjects. Cardiac vagal tone was defined as the chang in R-R interval after complete cholinergic blockade by atropine. Baroreflex sensitivity was determined with the "Oxford-method": R-R interval was regressed against systolic pressure. The interindividual correlation between cardiac vagal tone and baroreflex sensitivity for falling pressures was found to be significant, but not close (R = 0.81, P = 0.002). In each subject, the baroreflex regression line for falling pressures was extrapolated to the post-atropine R-R interval level; 50 mmHg was considered as minimum and 80 mmHg as maximum threshold level for the integrated baroreflex. From the relation between the individual regression lines and the minimum and maximum threshold levels, it was concluded that cardiac vagal tone could be generated by both baroreflex-dependent and -independent mechanisms, the ratio of which varies in different individuals, with the baroreflex-dependent mechanism being the dominant factor.

Adult↗
PubMed1995

Daily spontaneous running attenuated the central gain of the arterial baroreflex.

Exercise training attenuates arterial baroreflex function. Mechanisms responsible may include an attenuated aortic baroreceptor reactivity (afferent mechanisms) and/or an attenuated central baroreflex gain. We tested the hypothesis that the aortic baroreceptor reactivity and/or central gain is attenuated by daily spontaneous running (DSR). Eighteen anesthetized Sprague-Dawley rats (11 control and 7 DSR) were tracheotomized and instrumented with femoral venous and right carotid arterial catheters. Electrodes were placed around the left aortic depressor nerve and the lumbar sympathetic trunk. Eight to thirteen weeks of DSR were associated with a 20% increase in heart weight-to-body weight ratio (2.83 +/- 0.04 vs. 3.39 +/- 0.10 g/kg; P < 0.001) and resting bradycardia (413 +/- 6 vs. 384 +/- 10 beats/min; P = 0.01). DSR reduced the central gain of the baroreflex regulation of heart rate (0.210 +/- 0.046 vs. 0.005 +/- 0.021 beats.min-1.%-1; P = 0.004) during decreases in arterial pressure. However, the reactivity of aortic baroreceptor afferents and the central gain of the baroreflex control of lumbar sympathetic nerve activity were not different in control and DSR rats. Thus DSR reduced the central gain of the arterial baroreflex regulation of heart rate without changing the reactivity of aortic baroreceptor afferents. We conclude that afferent mechanisms are not responsible for the training-induced reduction in arterial baroreflex function.

Animals↗
PubMed1995

Cardiopulmonary baroreceptors modulate carotid baroreflex control of heart rate during dynamic exercise in humans.

Numerous studies have reported that, at rest, maximal carotid baroreflex gain is modulated by cardiopulmonary baroreceptors. The purpose of this study was to measure the maximal gain for carotid baroreflex control of heart rate (HR) and blood pressure [mean arterial pressure (MAP)] during dynamic exercise alone and when exercise was accompanied by two levels of cardiopulmonary baroreceptor unloading. Lower body negative pressure (LBNP) produced similar reductions in central venous pressure (CVP) at rest and during exercise. Baroreflex gain for HR at rest was not affected by low-level LBNP but was significantly increased by high-level LBNP [-0.31 +/- 0.05 to -0.57 +/- 0.23 beats.min-1.mmHg-1 carotid sinus pressure (CSP), no LBNP vs. high-level LBNP, P < 0.05]. Exercise combined with low- and high-level LBNP resulted in reflex HR gains (-0.83 +/- 0.44 and -0.83 +/- 0.17 beats.min-1.mmHg-1 CSP, low- vs. high-level LBNP, P < 0.05) that were significantly greater than the algebraic sum of the HR gain measured during exercise and LBNP alone. Neither exercise nor the two levels of LBNP significantly altered baroreflex gain for MAP. The slope relating HR gain to CVP at rest was significant (0.07 +/- 0.02 beats.min-1.mmHg CSP-1.mmHg CVP-1, P < 0.01) and increased 114% during exercise (P < 0.05). A similar analysis of MAP gain found no difference in slope between rest and exercise (P > 0.05). Together these data indicate 1) a tonic inhibitory interaction between cardiopulmonary baroreceptors and carotid baroreflex control of HR during exercise, and 2) a nonlinear relationship between deactivation of cardiopulmonary baroreceptors and changes in carotid baroreflex gain. This interaction may improve overall cardiovascular regulation when central blood volume and/or CVP is reduced, as has been reported during prolonged exercise in the heat.

Adult↗
PubMed1995

Methodology of spontaneous baroreflex relationship assessed by surrogate data analysis.

We tested the hypothesis that the spontaneous beat-by-beat interactions of systolic blood pressure (SBP) and R-R interval reflected true baroreflex events rather than chance interactions. Original data sets of 1,024 heartbeats obtained in seated rest from six healthy subjects [R-R interval = 953 +/- 94 (+/- SE) ms] were compared with isospectral [generated by a windowed (inverse) Fourier transform with phase randomization] and isodistribution (data points randomly shuffled) surrogate data sets. The isospectral data set was used to test for random phase relationships, and the isodistribution data set was used for effects of white noise between SBP and R-R interval. Spontaneous baroreflex sequences were defined as three or more beats in which SBP and the R-R interval of the same (lag 0), next (lag 1), or next following (lag 2) beat changed in the same direction. The total number of baroreflex sequences in the original data was significantly greater than the surrogates (P < 0.001). In the original data, there were significantly (P < 0.001) more lag 0 than lag 1 or lag 2 baroreflex sequences. Therefore, these results indicated that spontaneous baroreflex sequences represented physiological rather than chance interactions and that baroreflex responses can occur within the same beat.

Adult↗
PubMed1996

Effect of vasopressin on baroreflex control of lumbar sympathetic nerve activity and hindquarter resistance.

Arginine vasopressin (AVP) has been shown to increase the inhibitory influence of the baroreflex on sympathetic nerve activity by a mechanism involving receptors located in the area postrema. The purpose of these experiments was to study the functional effect of this action of AVP by testing the hypothesis that AVP can buffer its own vasoconstrictor effect by facilitating baroreflex-mediated withdrawal of sympathetic nerve activity. Specifically, we determined 1) if AVP can attenuate increases in hindquarter vascular resistance during the infusion of another vasoconstrictor, phenylephrine, and 2) whether the effects of AVP on vascular resistance are associated with appropriate corresponding changes in lumbar sympathetic nerve activity (LSNA). In pentobarbital-anesthetized New Zealand White rabbits the baroreflex was stimulated by phenylephrine-induced elevations in arterial pressure. Baroreflex-mediated changes in heart rate (HR), calculated hindquarter vascular resistance index (R), and LSNA were determined during the simultaneous intravertebral infusion of AVP (0, 0.5, or 1.0 ng.kg-1, min-1). Intravertebral infusion of AVP alone had no effect on resting mean arterial pressure (MAP) but reduced baseline values for LSNA and HR. Intravenous infusion of phenylephrine alone produced dose-dependent increases in MAP and R and decreases in LSNA and HR. The simultaneous infusion of AVP (0.5 or 1.0 ng.kg-1 min-1) and phenylephrine (1.25, 2.5, 5.0, 7.5, and 10.0 micrograms.kg-1.min-1) had no effect on the increase in MAP but attenuated the increases in R and facilitated the reductions in LSNA at all doses of phenylephrine. The higher dose of AVP also enhanced the phenylephrine-induced reductions in HR. In contrast, the intravenous infusion of AVP (1.0 ng.kg-1.min-1) did not alter baroreflex-mediated changes in R, LSNA, or HR. Therefore, we conclude that the action of AVP to increase baroreflex-mediated sympathoinhibition results in an attenuated rise in hindquarter vascular resistance during the infusion of another vasoconstrictor, phenylephrine.

Animals↗
PubMed1996

Invariance of the resistance to venous return to carotid sinus baroreflex control.

Despite the well-established fact that the carotid sinus baroreflex system has profound control over the physical properties of the systemic circulation, the resistance to venous return (RVR) seems to be invariant of such control. We hypothesized that this apparent paradox may be explained from the baroreflex changes in systemic arterial compliance. In 12 pentobarbital-anesthetized mongrel dogs, RVR was measured at controlled carotid sinus pressures (CSP) of 50 and 200 mmHg with normal and artificially increased arterial compliance. Arterial compliance was determined from the arterial pressure decay when systemic blood flow was stopped with total vena caval occlusion. Changing CSP between 50 and 200 mmHg changed RVR significantly only under the condition of artificially increased arterial compliance. A four-parameter lumped model of the systemic circulation revealed that the baroreflex changes in arterial compliance and arterial resistance, which occurred in opposite directions, prevented a change in RVR when CSP was changed. The data also suggested that approximately 75% of RVR was attributed to large and conduit veins, the resistances along which were insensitive to baroreflex control. We concluded that the invariance of RVR results from a combination of 1) baroreflex change in the arterial compliance, 2) baroreflex insensitivity of the resistance along large and conduit veins, and 3) spatially distinct location between the major site of reflex change in capacitance and the major site of compliance.

Animals↗
PubMed1996

Baroreflex frequency-response characteristics to aortic depressor and carotid sinus nerve stimulation in rats.

Dynamic cardiovascular regulation depends on baroreflexes and the processing of sensory information. We evaluated the influence of choice of anesthetic on the frequency-response characteristics of the baroreflex of rats by electrical stimulation of two major baroreceptor-containing nerves, the carotid sinus (CSN) and aortic depressor nerves (ADN). The ADN contains baroreceptors alone, and the CSN has both chemoreceptors and baroreceptors. Most studies were performed under pentobarbital sodium (PB; 65 mg/kg) anesthesia. We compared this to a combination of alpha-chloralose (80 mg/kg) and urethan (800 mg/kg) (CU). Stimulus trains were fixed at 60-s periods (0.1-ms shocks, supramaximal intensities, 1-200 Hz) and delivered in steady and burst patterns. Unilateral steady-frequency ADN stimulation in PB-anesthetized rats evoked reflex decreases in mean arterial pressure and heart rate that increased with frequencies between 1 and approximately 10 Hz before reaching a maximum. From 10 to 200 Hz, PB ADN reflex responses were sustained at these maximal levels. Cutting the opposite ADN or both CSNs did not alter ADN baroreflex relationships. Heart rate and mean arterial pressure depressor responses evoked by CSN stimulation in PB-anesthetized rats were smaller compared with ADN stimulation and were biphasic, with small pressor responses at 1 Hz. Maximal CSN depressor responses in PB-anesthetized rats occurred at approximately 20 Hz and were sustained at 20-200 Hz. Baroreflex responses for ADN stimulation in CU-anesthetized rats were similar to those in PB-anesthetized rats. In contrast, in CU-anesthetized rats, maximal CSN responses occurred at 20 Hz but declined at 50-200 Hz. Constant- and burst-stimulation responses were equivalent. The results suggest that rat aortic baroreflex responses are sustained even at very high input frequencies (> 100 Hz). The sustained high-frequency baroreflex responses seem to present a paradox in understanding central integration because other studies show substantial depression of sensory transmission at the first synapse in the nucleus tractus solitarius at frequencies as low as 10 Hz.

Animals↗
PubMed1996

Frequency and amplitude of sympathetic discharges by baroreflexes during hypoxia in conscious rabbits.

Sympathetic nerve activity (SNA) from multifiber preparations exhibits two distinct components: the frequency at which discharges occur and their relative amplitude (reflecting the number of activated nerve fibers within each burst). These two components may respond independently to various afferent inputs, indicating separate central controlling processes. We examined the response in the frequency and amplitude of renal SNA to changes in baroreceptor activity and the effect of two forms of hypoxia on this relationship in nine conscious rabbits. Rabbits breathed either room air or one of two hypoxic gas mixtures (10% O2 or 10% O2 + 3% CO2) for 20 min, during which baroreflexes were stimulated by ramp increases and then decreases in arterial pressure with phenylephrine (0.5 mg/ml iv) and nitroprusside (1 mg/ml) (total arterial pressure range induced was 80 mmHg). Hypoxia with 10% O2 significantly increased the resting frequency of SNA before baroreflex modifications from 2.15 +/- 0.18 to 2.82 +/- 0.25 discharges/s and with 10% O2 + 3% CO2 to 3.20 +/- 21 discharges/s. The amplitude of sympathetic discharges was increased 44 +/- 5% over control levels during 10% O2 but was not further increased by the addition of 3% CO2. The baroreflex curve for total SNA (1-s averages of the integrated neurogram) showed a graded response to the two hypoxic stimuli, with significant increases in the upper plateau, gain, and resting point on the curves. However, the baroreflex curve for the frequency or amplitude of sympathetic discharges did not show graded responses to each hypoxic treatment. The frequency baroreflex curve was sigmoidal and not changed from air during 10% O2. During 10% O2 + 3% CO2, the gain (responsiveness) of the curve was increased although the range of frequencies occurring was unaltered. The baroreflex curve for the amplitude showed similar responses to the two hypoxic stimuli, namely, increases in the upper plateau, gain, and resting point of the curve. We conclude that the frequency and amplitude of sympathetic discharges are able to respond differentially to changes in afferent stimuli. Given that alterations in the frequency and recruitment of sympathetic fibers (amplitude) to the kidney may have differing effects, this phenomenon may provide a previously unknown level of renal hemodynamic control through the interaction of specific afferent inputs to the central nervous system.

Animals↗
PubMed1998

Reduction in arterial compliance alters carotid baroreflex control of cardiac output in a model of hypertension.

Baroreflex regulation of cardiac output is determined by the performance of the heart as well as the available blood flow returning to the heart (i.e., venous return). We hypothesized that a decrease in arterial compliance (C(a)) would affect carotid baroreflex control of cardiac output by altering the slope of the venous return curve (VR curve). Baroreflex control of systemic arterial pressure (Pa), central venous pressure (Pv), heart rate, cardiac output (CO), and peripheral vascular resistance (R) were determined during bilateral carotid occlusion (BCO) in spontaneously hypertensive (hypertensive, HT) and Sprague-Dawley (normotensive, NT) rats. C(a) was determined from the rate of arterial pressure decay when CO was transiently stopped, and the VR curve was obtained during graded inflation of a vascular balloon positioned in the right atrium. The inverse slope of the VR curve was used as an index of the resistance to venous return (RVR). The baseline slope of the VR curve was -50.5 +/- 3.3 vs. -35.5 +/- 2.6 ml.kg-1.min-1.mmHg-1 in NT vs. HT, respectively (P < 0.05). Control values of Pa (96 +/- 5 vs. 124 +/- 8 mmHg) and R [0.43 +/- 0.04 vs. 0.80 +/- 0.07 peripheral resistance units (PRU)] were reduced in NT, whereas Ca (0.062 +/- 0010 vs. 0.036 +/- 0.003 ml.kg-1.mmHg-1) was elevated in NT vs. HT, respectively (P < 0.05). Analysis of the pressure dependence of C(a) demonstrated that C(a) was a nonlinear function of Pa, and the exponential decay constant for the C(a)-Pa relationship was reduced in HT (0.0055 +/- 0.0012 vs. 0.0012 +/- 0.0002 min, NT vs. HT, P < 0.05). Baroreflex activation by BCO significantly increased Pa (delta Pa, 20 +/- 4 vs. 28 +/- 3 mmHg) and R (delta R, 0.16 +/- 0.04 vs. 0.24 +/- 0.06 PRU) in NT vs. HT, respectively. However, BCO significantly decreased CO in NT but not HT (delta CO, -24 +/- 5 vs. -4 +/- 6 ml.kg-1.min-1, P < 0.05). In NT, RVR was increased 39 +/- 9% during BCO (P < 0.05), whereas RVR increased 8 +/- 3% in HT (P = NS). From these findings, we conclude that the difference in baroreflex control of CO is mediated, in part, by the reduction in C(a), which minimized the baroreflex-evoked increase in RVR.

Animals↗
PubMed2000

Effects of central infusion of ANG II and losartan on the cardiac baroreflex in rabbits.

The effect of chronic activation or inhibition of central ANG II receptors on cardiac baroreflex function in conscious normotensive rabbits was examined. Animals received a fourth ventricular (4V) infusion of ANG II (30 and 100 ng/h), losartan (3 and 30 microg/h), or Ringer solution (2 microl/h) for 2 wk. After 1 and 2 wk, ANG II (100 ng/h) decreased cardiac baroreflex gain by 20 and 37%, respectively (P = 0.015), whereas losartan (30 microg/h) increased baroreflex gain by 24 and 58%, respectively (P = 0.02). Within 1 wk of the end of the infusions, cardiac baroreflex gain had returned to control. Ringer solution or the lower doses of ANG II or losartan did not modify the cardiac baroreflex function. Blood pressure and heart rate were not altered by any treatment, nor was their variability affected. These data demonstrate a novel long-term modulation of cardiac baroreflexes by endogenous ANG II that is independent of blood pressure level.

Angiotensin II↗