Component Of Baroreflex Research Articles

The nonpharmacological sequence method provides a reliable evaluation of baroreflex sensitivity in fish.

The most commonly used technique to study the barostatic regulation of blood pressure in ectothermic vertebrates consists of determining the heart rate response to pharmacological manipulations of blood pressure, the so-called "Oxford method."Although well established, the Oxford method has some important limitations, such as induction of hypervolemia in small animals and undesired effects of vasoactive drugs on central and peripheral baroreflex components. As an alternative, the sequence method, which consists in the computerized evaluation of naturally-occurring baroreflex adjustments of heart rate without the need for pharmacological administrations, was developed to study baroreflexes. In the present study, we compare this sequence method with the Oxford technique in two teleost species with different life styles, and we assess the optimal software configuration for the employment of the sequence method in fish. Calculation of baroreflex gain through the sequence method was adequate and reliable when the software was configured to search for baroreflex sequences with a minimum length of three cardiac cycles with a delay of one cardiac cycle between fluctuations in mean ventral aortic blood pressure and reflex changes in pulse interval. When properly configured, the sequence and the Oxford methods yielded similar determinations of the baroreflex gain in fish.

Bed nucleus of the stria terminalis modulates baroreflex cardiac activity: an interaction between alpha-1 receptors and NMDA/nitric oxide pathway.

The bed nucleus of the stria terminalis (BNST) is a forebrain structure, involved in the modulation of neuroendocrine, cardiovascular and autonomic responses. One of the responses is baroreflex activity, which consists in a neural mechanism responsible for keeping the blood pressure within a narrow range of variation. It has been reported that blockade of BNST α1-adrenoceptors increased the bradycardic component of baroreflex. In addition, such receptors are able to modulate glutamate release in this structure. Interestingly, BNST NMDA receptor antagonism and neuronal nitric oxide synthase (nNOS) inhibition led to the same effect of the α1-adrenoceptors blockade on baroreflex bradycardic response. Therefore, the hypothesis of the present study is that BNST noradrenergic transmission interacts with NMDA/NO pathway through α1 adrenoceptors to modulate the baroreflex activity. Male Wistar rats had stainless steel guide cannulas bilaterally implanted in the BNST. Subsequently, a catheter was inserted into the femoral artery for cardiovascular recordings, and into the femoral vein for assessing baroreflex activation. Injection of the noradrenaline reuptake inhibitor reboxetine in the BNST did not modify the tachycardic, but significantly decreased the bradycardic component of baroreflex. Administration of an α1, but not an α2 antagonist into the BNST prior to reboxetine prevented this effect. Likewise, previous injection of NMDA/NO pathway blockers inhibited the effect of reboxetine on bradycardic response. In conclusion, it was demonstrated for the first time the existence of an interaction between BNST noradrenergic, glutamatergic and nitrergic neurotransmissions in the modulation of bradycardic baroreflex response.

Role of the HPA Axis in the Metabolic and Baroreflex Components of Hypoglycemia-Associated Autonomic Failure.

Role of the HPA Axis in the Metabolic and Baroreflex Components of Hypoglycemia-Associated Autonomic Failure.

Adaptive Mechanisms of Baroreflectory Regulation of the Cardiovascular System in Extreme Hyperoxia

The cardiovascular system of vertebrates, including humans, is well known to respond to hyperoxia by vasoconstriction, bradycardia and decreased contractility of the left heart ventricle. We hypothesized that all of these responses are components of the baroreflex that regulates blood pressure and circulation in hyperoxia. To test this hypothesis, we carried out experiments on awake rats in which the dynamics of arterial blood pressure, organ blood flow (brain, kidney, lower limbs) and ECG was tracked in response to oxygen breathing at 1, 3 and 5 ATA. The afferent and efferent baroreflex pathways were studied using denervation of the carotid baroreceptors and transection of the aortic depressor nerves and vagus nerve. The baroreflex effectiveness was assessed using phenylephrine injections or spontaneous changes in blood pressure. To activate the GABAergic system, nipecotic acid was injected into the lateral ventricle of the brain. Our studies demonstrated the presence of all the baroreflex components in hyperoxia which were triggered by a sharp rise in blood pressure due to systemic vasoconstriction. Hyperoxic vasoconstriction, in turn, arose due to endothelium-derived nitric oxide (NO) which binds to superoxide anions followed by a loss of the vasodilator component of vascular tone. Aortic and carotid sinus baroreceptors with ascending nerve fibers were identified as an afferent component of the hyperoxic baroreflex. Bradycardia and a decrease in cardiac output, resulting from baroreflex activation by hyperoxia, are actualized via efferent sympathetic and parasympathetic pathways. At 1 and 3 ATA the baroreflex effectiveness increased compared to atmospheric air breathing, but extreme hyperoxia (5 ATA) suppressed the baroreflex mechanism. Activation of the GABAergic system in the cerebral cortex by nipecotic acid prevented the loss of the hyperoxic baroreflex. In hyperoxia, the baroreflex mechanism realizes adaptive responses of the cardiovascular system aimed at restraining the delivery of excess oxygen to an organism and mitigates activation of the sympathetic nervous system.

Assessing Synergy/Redundancy of Baroreflex and Non-Baroreflex Components of the Cardiac Control during Sleep.

Cardiovascular regulation and autonomic function change across sleep stages and compared to wake. Little information is present in literature about cardiac control during sleep especially in relation to new information-theoretic quantities such as synergy and redundancy. In the present work we compute synergy and redundancy of baroreflex and non-baroreflex components of the cardiac control according to two information-theoretic approaches, namely predictive information decomposition (PID) and minimal mutual information (MMI) methods. We applied a bivariate approach to heart period (HP) and systolic arterial pressure (SAP) beat-to-beat variability series during sleep in a healthy subject. PID approach computes the net balance between synergy and redundancy, while MMI calculates the two quantities as separate entities. Results suggested that: i) redundancy was dominant over synergy during NREM phases; ii) redundancy increased during NREM phase; iii) synergy did not change across the sleep stages. We interpret this result as a consequence of the vagal enhancement, slowing and deepening of respiration during NREM phases. These preliminary findings support the potential of assessing redundancy/synergy of baroreflex-related and unrelated regulations during sleep to improve our knowledge about physiological mechanisms.

The medial preoptic area modulates autonomic function under resting and stress conditions

The medial preoptic area (mPOA) participates in the temperature and cardiovascular control. The mPOA receives inputs from limbic structures and sends projections to hypothalamus and brainstem. Moreover, stress elicits pronounced neuronal activation in mPOA, suggesting its involvement in central neural pathway mediating stress responses. In the present study, we report the effect of acute mPOA neurotransmission inhibition using cobalt chloride (CoCl2-nonselective synapse blocker) on the mean arterial pressure (MAP), heart rate (HR), body and tail temperature (Tbody and Ttail, respectively), as well as on the HR component of baroreflex. We also verified the participation of mPOA in the autonomic changes evoked by acute restraint stress (RS). Our results demonstrated that microinjection of CoCl2 into mPOA caused tachycardia, hyperthermia and a Ttail decrease, without altering MAP. The inhibition of mPOA with CoCl2 increased the sympathetic component of cardiac baroreflex when assessed 10min after its administration. In addition, pretreatment of mPOA with CoCl2 increased RS-evoked tachycardic and hyperthermic responses evoked by RS when compared with aCSF-treated animals, without affecting the RS-evoked pressor response and the fall in Ttail. In summary, our results suggest that mPOA exerts a tonic inhibitory influence on the sympathetic cardiac tone under both rest and stress conditions, modulating negatively the sympathetic component of baroreflex. Results also confirm the mPOA involvement in the control of body temperature because its inhibition was followed by a sustained increase in body temperature and vasoconstriction in the tail artery territory.

Effect of salt loading on baroreflex sensitivity in reduced renal mass hypertension

ABSTRACTBackground: High dietary salt, as well as renal mass reduction, is known to decrease baroreflex sensitivity in rats. However, the effect of high salt intake on baroreflex sensitivity is unknown in reduced renal mass (RRM) hypertension; therefore, the aim of this study was to investigate the effects of salt loading on arterial baroreflex sensitivity and mean arterial pressure (MAP) in RRM hypertension.Methods: Both RRM and sham-operated control (SO) rats were loaded with 0.25 or 0.5% NaCl for five weeks. Plasma Na+, K+, and creatinine levels were measured, and baroreflex sensitivity was evaluated before and after β1 blockade. In addition, cardiac vagal tone and intrinsic heart rate (IHR) were measured. RESULTS: RRM decreased full baroreflex sensitivity of the tachycardic response under 0.5% NaCl loading and the parasympathetic bradycardic response under 0% NaCl loading. The NaCl loading did not affect the severity of RRM hypertension. Cardiac vagal tone and IHR decreased in RRM rats versus SO controls under all NaCl loading conditions. RRM decreased plasma K+ under 0% NaCl loading and increased plasma Na+ under 0.5% NaCl loading. High (0.5%) NaCl loading decreased IHR and increased plasma creatinine and left ventricular weight in RRM rats. CONCLUSIONS: RRM in combination with 0.5% NaCl loading led to a decrease in the sensitivity of full baroreflex and of the parasympathetic component of baroreflex. Changes in plasma Na+ and K+ levels, due to NaCl loading, may have contributed to the decrease in baroreflex sensitivities and IHR but had no effect upon MAP in RRM rats.

Dynamic Modulation of Spontaneous Cardiac Baroreflex Sensitivity to Changes in Workloads in Humans

The arterial baroreflex plays important role in cardiovascular regulations during exercise. Previous studies showed that the spontaneous sensitivity of the cardiac component of arterial baroreflex (SBRS) is progressively attenuated with increasing workloads of dynamic exercise. However, dynamic modulation of SBRS to changes in workloads is unknown. PURPOSE: We aimed to investigate the amplitude response and phase response of SBRS during cycling exercise with sinusoidally-varying workload. METHODS: We studied 8 healthy male volunteers. After 5 minutes of resting measurements, the subjects performed cycling exercise at 50 W for 5 minutes. Then the workload was changed in a sinusoidal pattern between 30 W to 70 W for 32 minutes. The periods of sinusoidal workload were set to 4, 8 and 16 minutes. Subjects performed each of those three sinusoidal load exercise on separate days in random order. SBRS was evaluated as the slopes of the linear relations between R-R interval and systolic arterial blood pressure (SAP) during spontaneous sequences of at least three consecutive beats when SAP and R-R interval changed in the same directions. SBRS for all sequences were superimposed every periods of sinusoidal load and fitted to a sine model using the least-squares error approach to calculate amplitude response and phase response. RESULTS: During sinusoidal exercise, SBRS changed sinusoidally with the change of workload. The amplitude response of SBRS for 4, 8 and 16 minutes periods were 1.4 ± 0.3, 1.4 ± 0.2, and 1.2 ± 0.3 msec/mmHg, respectively and were not significantly different (p > 0.05). The phase lag of the SBRS from the sinusoidally-varying workload for 4, 8 and 16 minutes periods were 20.4 ± 4.2, 17.4 ± 4.3, and 3.6 ± 4.2 degrees, respectively. The phase lag of the SBRS in 16 minutes period was significantly smaller compared to 4 minutes period (p < 0.05). CONCLUSIONS: We conclude that the arterial baroreflex control of heart periods is modulated continuously in response to changes in workload. When workload changes fast, the modulation of SBRS delays from the changes in workloads. However, SBRS is modulated with almost no delay in response to relatively slow changes in workloads. We suggest that the dynamic modulation of the SBRS is one of the mechanisms to regulate cardiovascular responses in accordance with changes in workloads.

Chronic intermittent hypoxia in rats enhances the respiratory-related sympatho-inhibitory component of baroreflex

Chronic intermittent hypoxia in rats enhances the respiratory-related sympatho-inhibitory component of baroreflex

Neuro-glial communication in NTS after hypoxia

Humans ascending to high altitudes are submitted to sustained hypoxia (SH), which activates the peripheral chemoreflex with several autonomic and respiratory responses. In this study we analyzed initially the effect of short-term SH (24 hours, FIO210%) on the processing of cardiovascular and respiratory reflexes using an in situ preparation of rats. SH increased both the sympatho-inhibitory and bradycardiac components of baroreflex and the sympathetic and respiratory responses of peripheral chemoreflex. The electrophysiological properties and synaptic transmission in the nucleus tractus solitarius (NTS) neurons, the first synaptic station of afferents of baro- and chemoreflexes, were evaluated using brainstem slices and whole-cell patch clamp. The 2nd-order NTS neurons were identified by previous application of fluorescent tracer onto carotid body for chemoreceptor afferents or onto aortic depressor nerve for baroreceptor afferents. SH increased the intrinsic excitability of NTS neurons. Delayed excitation, caused by A-type potassium current (IKA), was observed in most of NTS neurons from control rats. The IKA amplitude was higher in identified 2nd-order NTS neurons from control than in SH rats. SH also blunted the astrocytic inhibition of IKA in NTS neurons and increased the synaptic transmission in response to afferent fibers stimulation. The frequency of spontaneous excitatory currents was also increased in neurons from SH rats, indicating that SH increased the neurotransmission by pre-synaptic mechanisms. We conclude that short-term SH changed the glia-neuron interaction, increasing the excitability and excitatory transmission of NTS neurons, which may contribute to the observed increase in the reflex sensitivity of baro- and chemoreflex in in situ preparation. Financial support: FAPESP and CNPq.

Brain angiotensin type 1 receptor activation play a crucial role in immune-inflammatory mechanisms of central sympathoexitation in hypertension and heart failure

selected for presentation 25.5 Chronic intermittent hypoxia in rats enhances the respiratoryrelated sympatho-inhibitory component of baroreflex D.J.A. Moraes, B.H. Machado Department of Physiology, University of Sao Paulo, Ribeirao Preto, SP,

Enhanced Firing in NTS Induced by Short-Term Sustained Hypoxia Is Modulated by Glia-Neuron Interaction

Humans ascending to high altitudes are submitted to sustained hypoxia (SH), activating peripheral chemoreflex with several autonomic and respiratory responses. Here we analyzed the effect of short-term SH (24 h, FIO210%) on the processing of cardiovascular and respiratory reflexes using an in situ preparation of rats. SH increased both the sympatho-inhibitory and bradycardiac components of baroreflex and the sympathetic and respiratory responses of peripheral chemoreflex. Electrophysiological properties and synaptic transmission in the nucleus tractus solitarius (NTS) neurons, the first synaptic station of afferents of baroreflexes and chemoreflexes, were evaluated using brainstem slices and whole-cell patch-clamp. The second-order NTS neurons were identified by previous application of fluorescent tracer onto carotid body for chemoreceptor afferents or onto aortic depressor nerve for baroreceptor afferents. SH increased the intrinsic excitability of NTS neurons. Delayed excitation, caused by A-type potassium current (IKA), was observed in most of NTS neurons from control rats. The IKA amplitude was higher in identified second-order NTS neurons from control than in SH rats. SH also blunted the astrocytic inhibition of IKA in NTS neurons and increased the synaptic transmission in response to afferent fibers stimulation. The frequency of spontaneous excitatory currents was also increased in neurons from SH rats, indicating that SH increased the neurotransmission by presynaptic mechanisms. Therefore, short-term SH changed the glia-neuron interaction, increasing the excitability and excitatory transmission of NTS neurons, which may contribute to the observed increase in the reflex sensitivity of baroreflex and chemoreflex in in situ preparation.

Baroreflex sensitivity: reliability of baroreflex components of the Valsalva maneuver.

The reliability of the baroreflex sensitivity measurement has not yet been established. Thus, the objective of this study was to define intra-rater reliability of baroreflex sensitivity (BRS) measurements of the Valsalva maneuver (VM) in healthy individuals. Twenty-two healthy volunteers underwent VM testing at two time points. Intra-rater reliability was determined by the intra-class correlation coefficient (ICC), standard error of measurement and minimal detectable difference. Vagal BRS showed good reliability (ICC=0.84), while alternative adrenergic BRS was moderately reproducible (ICC=0.61). Vagal and alternative adrenergic components of BRS in VM are reliable measurements.

Discharges of aortic and carotid sinus baroreceptors during spontaneous motor activity and pharmacologically evoked pressor interventions.

Our laboratory has demonstrated that the cardiomotor component of aortic baroreflex is temporarily inhibited at the onset of spontaneous motor activity in decerebrate cats, without altering carotid sinus baroreflex. A reason for this dissociation may be attributed to a difference in the responses between aortic nerve activity (AoNA) and carotid sinus nerve activity (CsNA) during spontaneous motor activity. The stimulus-response curves of AoNA and CsNA against mean arterial blood pressure (MAP) were compared between the pressor interventions evoked by spontaneous motor activity and by intravenous administration of phenylephrine or norepinephrine, in which the responses in heart rate (HR) were opposite (i.e., tachycardia vs. baroreflex bradycardia), despite the identical increase in MAP of 34-40 mmHg. In parallel to the pressor response, mean AoNA and CsNA increased similarly by 78-81 and by 88 % of the baseline control, respectively, irrespective of whether the pressor response was evoked by spontaneous motor activity or by a pharmacological intervention. The slope of the stimulus-response curve of the mean AoNA became greater (P < 0.05) during spontaneous motor activity as compared to the pharmacological intervention. On the other hand, the stimulus-response curve of the mean CsNA and its slope were equal (P > 0.05) between the two pressor interventions. Furthermore, the slopes of the stimulus-response curves of both diastolic AoNA and CsNA (defined as the minimal value within a beat) exhibited a greater increase during spontaneous motor activity. All differences in the slopes of the stimulus-response curves were abolished by restraining HR at the intrinsic cardiac frequency. In conclusion, mean mass activities of both aortic and carotid sinus baroreceptors are able to encode the beat-by-beat changes in MAP not only at rest but also during spontaneous motor activity and spontaneous motor activity-related reduction of aortic baroreceptor activity is denied accordingly.

Signal transduction of aortic and carotid sinus baroreceptors is not modified by central command during spontaneous motor activity in decerebrate cats

Our laboratory has suggested that central command provides selective inhibition of the cardiomotor component of aortic baroreflex at the start of exercise, preserving carotid sinus baroreflex. It is postulated that central command may modify the signal transduction of aortic baroreceptors, so as to decrease aortic baroreceptor input to the cardiovascular centers, and, thereby, can cause the selective inhibition of aortic baroreflex. To test the hypothesis, we directly analyzed the responses in multifiber aortic nerve activity (AoNA) and carotid sinus nerve activity (CsNA) during spontaneous motor activity in decerebrate, paralyzed cats. The increases of 62-104% in mean AoNA and CsNA were found during spontaneous motor activity, in proportion to a rise of 35 ± 3 mmHg (means ± SE) in mean arterial blood pressure (MAP), and had an attenuating tendency by restraining heart rate (HR) at the lower intrinsic frequency of 154 ± 6 beats/min. Brief occlusion of the abdominal aorta was conducted before and during spontaneous motor activity to produce a mechanically evoked increase in MAP and, thereby, to examine the stimulus-response relationship of arterial baroreceptors. Although the sensitivity of the MAP-HR baroreflex curve was markedly blunted during spontaneous motor activity, the stimulus-response relationships of AoNA and CsNA were not influenced by spontaneous motor activity, irrespective of the absence or presence of the HR restraint. Thus, it is concluded that aortic and carotid sinus baroreceptors can code beat-by-beat blood pressure during spontaneous motor activity in decerebrate cats and that central command is unlikely to modulate the signal transduction of arterial baroreceptors.

Electrophysiological properties of medullary neurons involved with sympatho-inhibitory component of baroreflex in rats submitted to chronic intermittent hypoxia

We evaluated whether or not CIH affect the sympatho-inhibitory pathway of the baroreflex. Male Wistar rats were submitted to CIH for 10 days while control rats were maintained in normoxia. Using the working heart-brainstem preparations we recorded respiratory and sympathetic activities as well as intracellular recordings of RVLM pre-sympathetic, CVLM and NTS neurons. Baroreflex was activated by stimulation of aortic depressor nerve (ADN) during inspiration or expiration. In control rats (n = 32), the inhibitory thoracic sympathetic nerve (tSN) reflex responses to ADN stimulation were more pronounced during expiration than during inspiration (P < 0.05). In CIH rats (n = 31) the magnitude of tSN (-87.4 ± 6 vs -71.5%; p < 0.05) inhibitory responses to ADN stimulation during expiration, but not inspiration, were larger than in controls. Also in CIH rats, RVLM and CVLM neurons that displayed expiratory modulation, exhibited larger inhibitory (-83 ± 5 vs -59 ± 3%; p < 0.05; n = 20) and excitatory (79 ± 3 vs 55 ± 4%; p < 0.05; n = 23) reflex responses, respectively, to ADN stimulation than in controls. In the presence of synaptic blockade, we did not observe any changes in the electrophysiological properties (excitability and input resistance) of RVLM and CVLM neurons of CIH and control rats. However, ADN stimulation during expiration produced a larger increase in the firing frequency of NTS neurons (109 ± 3 vs 35 ± 2%; p < 0.05; n = 25) in CIH than in control rats. These data indicate that the increased baroreflex sympatho-inhibitory responses during expiration of CIH rats are not related to changes in the intrinsic properties of RVLM pre-sympathetic and CVLM neurons, but are linked to changes in the synaptic transmission or electrophysiological properties of NTS neurons.

Detecting physiological systems with laser speckle perfusion imaging of the renal cortex

Laser speckle perfusion imaging (LSPI) has become an increasingly popular technique for monitoring vascular perfusion over a tissue surface. However, few studies have utilized the full range of spatial and temporal information generated by LSPI to monitor spatial properties of physiologically relevant dynamics. In this study, we extend the use of LSPI to analyze renal perfusion dynamics over a spatial surface of ~5 × 7 mm of renal cortex. We identify frequencies related to five physiological systems that induce temporal changes in renal vascular perfusion (cardiac flow pulse, respiratory-induced oscillations, baroreflex components, the myogenic response, and tubuloglomerular feedback) across the imaged surface and compare the results with those obtained from renal blood flow measurements. We find that dynamics supplied from global sources (cardiac, respiration, and baroreflex) present with the same frequency at all locations across the imaged surface, but the local renal autoregulation dynamics can be heterogeneous in their distribution across the surface. Moreover, transfer function analysis with forced blood pressure as the input yields the same information with laser speckle imaging or renal blood flow as the output during control, intrarenal infusion of N(ω)-nitro-L-arginine methyl ester to enhance renal autoregulation, and intrarenal infusion of the rho-kinase inhibitor Y-27632 to inhibit vasomotion. We conclude that LSPI measurements can be used to analyze local as well as global renal perfusion dynamics and to study the properties of physiological systems across the renal cortex.

Postural influences on the mechanical and neural components of the cardiovagal baroreflex

The ability to maintain arterial blood pressure when faced with a postural challenge has implications for the occurrence of syncope and falls. It has been suggested that posture-induced declines in the mechanical component of the baroreflex response drive reductions in cardiovagal baroreflex sensitivity associated with postural stress. However, these conclusions are largely based upon spontaneous methods of baroreflex assessment, the accuracy of which has been questioned. Therefore, the aim was to engage a partially open-loop approach to explore the influence of posture on the mechanical and neural components of the baroreflex. In nine healthy participants, we measured continuous blood pressure, heart rate, RR interval and carotid artery diameter during supine and standing postures. The modified Oxford method was used to quantify baroreflex sensitivity. In response to falling pressures, baroreflex sensitivity was similar between postures (P = 0.798). In response to rising pressures, there was an attenuated (P = 0.042) baroreflex sensitivity (mean ± SE) in the standing position (-0.70 ± 0.11 beats min(-1) mmHg(-1)) compared with supine (-0.83 ± 0.06 beats min(-1) mmHg(-1)). This was explained by a diminished (P = 0.016) neural component whilst standing (-30.17 ± 4.16 beats min(-1) mm(-1)) compared with supine (-38.23 ± 3.31 beats min(-1) mm(-1)). These effects were consistent when baroreflex sensitivity was determined using RR interval. Cardiovagal baroreflex sensitivity in response to rising pressures is reduced in young individuals during postural stress. Our data suggest that the mechanical component is unaffected by standing, and the reduction in baroreflex sensitivity is driven by the neural component.

Short-term variability of blood pressure: effects of lower-body negative pressure and long-duration bed rest

Mild lower-body negative pressure (LBNP) has been utilized to selectively unload cardiopulmonary baroreceptors, but there is evidence that arterial baroreceptors can be transiently unloaded after the onset of mild LBNP. In this paper, a black box mathematical model for the prediction of diastolic blood pressure (DBP) variability from multiple inputs (systolic blood pressure, R-R interval duration, and central venous pressure) was applied to interpret the dynamics of blood pressure maintenance under the challenge of LBNP and in long-duration, head-down bed rest (HDBR). Hemodynamic recordings from seven participants in the WISE (Women's International Space Simulation for Exploration) Study collected during an experiment of incremental LBNP (-10 mmHg, -20 mmHg, -30 mmHg) were analyzed before and on day 50 of a 60-day-long HDBR campaign. Autoregressive spectral analysis focused on low-frequency (LF, ~0.1 Hz) oscillations of DBP, which are related to fluctuations in vascular resistance due to sympathetic and baroreflex regulation of vasomotor tone. The arterial baroreflex-related component explained 49 ± 13% of LF variability of DBP in spontaneous conditions, and 89 ± 9% (P < 0.05) on day 50 of HDBR, while the cardiopulmonary baroreflex component explained 17 ± 9% and 12 ± 4%, respectively. The arterial baroreflex-related variability was significantly increased in bed rest also for LBNP equal to -20 and -30 mmHg. The proposed technique provided a model interpretation of the proportional effect of arterial baroreflex vs. cardiopulmonary baroreflex-mediated components of blood pressure control and showed that arterial baroreflex was the main player in the mediation of DBP variability. Data during bed rest suggested that cardiopulmonary baroreflex-related effects are blunted and that blood pressure maintenance in the presence of an orthostatic stimulus relies mostly on arterial control.

Diurnal Variation in the Mechanical and Neural Components of the Baroreflex

Diminished baroreflex sensitivity in the morning negatively influences morning coronary blood flow and blood pressure control in hypertensive patients. Our aim was to determine the contribution of the mechanical and neural components of the cardiac baroreflex to diurnal variation in blood pressure control. In 12 healthy participants, we used the modified Oxford method to quantify baroreflex sensitivity for rising (G(up)) and falling (G(down)) pressures in the morning (7:00 am) and afternoon (4:00 pm). Beat-to-beat blood pressure, R-R intervals, and carotid artery diameter measurements were recorded. Integrated sensitivity was determined by plotting R-R intervals against systolic blood pressure. The mechanical component was carotid artery diameter plotted against systolic blood pressure, and the neural component was R-R intervals plotted against carotid artery diameter. Linear mixed models were used to compare the integrated, mechanical, and neural sensitivities between morning and afternoon. We found significant diurnal variation in integrated sensitivity, with an attenuated response in the morning (G(up)=13.0±0.6; G(down)=6.3±0.4 ms/mm Hg) when compared with the afternoon (G(up)=15.1±0.6; G(down)=12.6±0.4 ms/mm Hg). For rising pressures, the diminished integrated sensitivity in the morning was caused by a reduction in mechanical sensitivity, whereas for falling pressures it was caused by a reduction in neural sensitivity. Our findings explicate the mechanisms underlying diurnal variation in baroreflex function. Pharmacological and lifestyle interventions targeted specifically at the diminished component of the cardiac baroreflex in the morning may lead to better management of hypertension.