The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study

2006 ◽  
Vol 291 (6) ◽  
pp. R1579-R1591 ◽  
Author(s):  
Sanja Milutinović ◽  
David Murphy ◽  
Nina Japundžić-Žigon
Keyword(s):  
Blood Pressure ◽  
Spectral Analysis ◽  
Low Frequency ◽  
Systolic Arterial Pressure ◽  
Short Term ◽  
Vasopressin Receptors ◽  
The Central Nervous System ◽  
Respiratory Stimulation ◽  
Stimulation Of

Although it has been suggested that vasopressin (VP) acts within the central nervous system to modulate autonomic cardiovascular controls, the mechanisms involved are not understood. Using nonpeptide, selective V1a, V1b, and V2 antagonists, in conscious rats, we assessed the roles of central VP receptors, under basal conditions, after the central application of exogenous VP, and after immobilization, on cardiovascular short-term variability. Equidistant sampling of blood pressure (BP) and heart rate (HR) at 20 Hz allowed direct spectral analysis in very-low frequency (VLF-BP), low-frequency (LF-BP), and high-frequency (HF-BP) blood pressure domains. The effect of VP antagonists and of exogenous VP on body temperature (Tb) was also investigated. Under basal conditions, V1a antagonist increased HF-BP and Tb, and this was prevented by metamizol. V1b antagonist enhanced HF-BP without affecting Tb, and V2 antagonist increased VLF-BP variability which could be prevented by quinapril. Immobilization increased BP, LF-BP, HF-BP, and HF-HR variability. V1a antagonist prevented BP and HR variability changes induced by immobilization and potentiated tachycardia. V1b antagonist prevented BP but not HR variability changes, whereas V2 antagonist had no effect. Exogenous VP increased systolic arterial pressure (SAP) and HF-SAP variability, and this was prevented by V1a and V1b but not V2 antagonist pretreatment. Our results suggest that, under basal conditions, VP, by stimulation of V1a, V1b, and cognate V2 receptors, buffers BP variability, mostly due to thermoregulation. Immobilization and exogenous VP, by stimulation of V1a or V1b, but not V2 receptors, increases BP variability, revealing cardiorespiratory adjustment to stress and respiratory stimulation, respectively.

Assessing baroreflex gain from spontaneous variability in conscious dogs: role of causality and respiration

2000 ◽  
Vol 279 (5) ◽  
pp. H2558-H2567 ◽  
Author(s):  
A. Porta ◽  
G. Baselli ◽  
O. Rimoldi ◽  
A. Malliani ◽  
M. Pagani
Keyword(s):  
High Frequency ◽  
Low Frequency ◽  
Systolic Arterial Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Parametric Models ◽  
Conscious Dogs ◽  
Regulatory Mechanisms ◽  
Stimulation Of

A double exogenous autoregressive (XXAR) causal parametric model was used to estimate the baroreflex gain (αXXAR) from spontaneous R-R interval and systolic arterial pressure (SAP) variabilities in conscious dogs. This model takes into account 1) effects of current and past SAP variations on the R-R interval (i.e., baroreflex-mediated influences), 2) specific perturbations affecting R-R interval independently of baroreflex circuit (e.g., rhythmic neural inputs modulating R-R interval independently of SAP at frequencies slower than respiration), and 3) influences of respiration-related sources acting independently of baroreflex pathway (e.g., rhythmic neural inputs modulating R-R interval independently of SAP at respiratory rate, including the effect of stimulation of low-pressure receptors). Under control conditions, αXXAR = 14.7 ± 7.2 ms/mmHg. It decreases after nitroglycerine infusion and coronary artery occlusion, even though the decrease is significant only after nitroglycerine, and it is completely abolished by total arterial baroreceptor denervation. Moreover, αXXAR is comparable to or significantly smaller than (depending on the experimental condition) the baroreflex gains derived from sequence, power spectrum [at low frequency (LF) and high frequency (HF)], and cross-spectrum (at LF and HF) analyses and from less complex causal parametric models, thus demonstrating that simpler estimates may be biased by the contemporaneous presence of regulatory mechanisms other than baroreflex mechanisms.

Hemodynamic regulation: investigation by spectral analysis

1985 ◽  
Vol 249 (4) ◽  
pp. H867-H875 ◽  
Author(s):  
S. Akselrod ◽  
D. Gordon ◽  
J. B. Madwed ◽  
N. C. Snidman ◽  
D. C. Shannon ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spectral Analysis ◽  
Pressure Fluctuations ◽  
Low Frequency ◽  
Cardiovascular Control ◽  
Respiratory Frequency ◽  
Atrial Pacing ◽  
Loop Model ◽  
Short Term ◽  
Renin Angiotensin

We investigated the hypothesis that beat-to-beat variability in hemodynamic parameters reflects the dynamic interplay between ongoing perturbations to circulatory function and the compensatory response of short-term cardiovascular control systems. Spontaneous fluctuations in heart rate (HR), arterial blood pressure, and respiration were analyzed by spectral analysis in the 0.02- to 1-Hz frequency range. A simple closed-loop model of short-term cardiovascular control was proposed and evaluated in a series of experiments: pharmacological blockades of the parasympathetic, alpha-sympathetic, beta-sympathetic, and renin-angiotensin systems were used to open the principal control loops in order to examine changes in the spectral pattern of the fluctuations. Atrial pacing was used to examine blood pressure variability in the absence of HR variability. We found that respiratory frequency fluctuations in HR are parasympathetically mediated and that blood pressure fluctuations at this frequency result almost entirely from the direct effect of centrally mediated HR fluctuations. The sympathetic nervous system appears to be too sluggish to mediate respiratory frequency variations. Low-frequency (0.02-0.09 Hz) fluctuations in HR are jointly mediated by the parasympathetic and beta-sympathetic systems and appear to compensate for blood pressure fluctuations at this frequency. Low-frequency blood pressure fluctuations are probably due to variability in vasomotor activity which is normally damped by renin-angiotensin system activity. Blockade of the alpha-adrenergic system, however, does not significantly alter low-frequency blood pressure fluctuations.

Frequency-dependent baroreflex modulation of blood pressure and heart rate variability in conscious mice

2005 ◽  
Vol 289 (5) ◽  
pp. H1968-H1975 ◽  
Author(s):  
Rubens Fazan ◽  
Mauro de Oliveira ◽  
Valdo José Dias da Silva ◽  
Luis Fernando Joaquim ◽  
Nicola Montano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Spectral Analysis ◽  
High Frequency ◽  
Low Frequency ◽  
Systolic Arterial Pressure ◽  
Pulse Interval ◽  
Sham Surgery ◽  
Cardiac Receptors

The goal of this study was to determine the baroreflex influence on systolic arterial pressure (SAP) and pulse interval (PI) variability in conscious mice. SAP and PI were measured in C57Bl/6J mice subjected to sinoaortic deafferentation (SAD, n = 21) or sham surgery ( n = 20). Average SAP and PI did not differ in SAD or control mice. In contrast, SAP variance was enhanced (21 ± 4 vs. 9.5 ± 1 mmHg2) and PI variance reduced (8.8 ± 2 vs. 26 ± 6 ms2) in SAD vs. control mice. High-frequency (HF: 1–5 Hz) SAP variability quantified by spectral analysis was greater in SAD (8.5 ± 2.0 mmHg2) compared with control (2.5 ± 0.2 mmHg2) mice, whereas low-frequency (LF: 0.1–1 Hz) SAP variability did not differ between the groups. Conversely, LF PI variability was markedly reduced in SAD mice (0.5 ± 0.1 vs. 10.8 ± 3.4 ms2). LF oscillations in SAP and PI were coherent in control mice (coherence = 0.68 ± 0.05), with changes in SAP leading changes in PI (phase = −1.41 ± 0.06 radians), but were not coherent in SAD mice (coherence = 0.08 ± 0.03). Blockade of parasympathetic drive with atropine decreased average PI, PI variance, and LF and HF PI variability in control ( n = 10) but had no effect in SAD ( n = 6) mice. In control mice, blockade of sympathetic cardiac receptors with propranolol increased average PI and decreased PI variance and LF PI variability ( n = 6). In SAD mice, propranolol increased average PI ( n = 6). In conclusion, baroreflex modulation of PI contributes to LF, but not HF PI variability, and is mediated by both sympathetic and parasympathetic drives in conscious mice.

Exploring directionality in spontaneous heart period and systolic pressure variability interactions in humans: implications in the evaluation of baroreflex gain

2005 ◽  
Vol 288 (4) ◽  
pp. H1777-H1785 ◽  
Author(s):  
Giandomenico Nollo ◽  
Luca Faes ◽  
Alberto Porta ◽  
Renzo Antolini ◽  
Flavia Ravelli
Keyword(s):  
Spectral Analysis ◽  
Spectral Component ◽  
Systolic Pressure ◽  
Low Frequency ◽  
Systolic Arterial Pressure ◽  
Phase Lag ◽  
Healthy Humans ◽  
Head Up Tilt ◽  
Causal Approach ◽  
Young Subjects

Although in physiological conditions RR interval and systolic arterial pressure (SAP) are likely to interact in a closed loop, the traditional cross-spectral analysis cannot distinguish feedback (FB) from feedforward (FF) influences. In this study, a causal approach was applied for calculating the coherence from SAP to RR ( Ks-r) and from RR to SAP ( Kr-s) and the gain and phase of the baroreflex transfer function. The method was applied, compared with the noncausal one, to RR and SAP series taken from 15 healthy young subjects in the supine position and after passive head-up tilt. For the low frequency (0.04–0.15 Hz) spectral component, the enhanced FF coupling ( Kr-s = 0.59 ± 0.21, significant in 14 subjects) and the blunted FB coupling ( Ks-r = 0.17 ± 0.17, significant in 4 subjects) found at rest indicated the prevalence of nonbaroreflex mechanisms. The tilt maneuver recovered FB influences ( Ks-r = 0.47 ± 0.16, significant in 14 subjects), which were stronger than FF interactions ( Ks-r = 0.34 ± 0.19, significant in 9 subjects). At the respiratory frequency, the RR-SAP regulation was balanced at rest ( Ks-r = 0.30 ± 0.18 and Kr-s = 0.29 ± 0.20, significant in 11 and 8 subjects) and shifted toward FB mechanisms after tilt ( Ks-r = 0.35 ± 0.19 and Kr-s = 0.19 ± 0.11, significant in 14 and 8 subjects). The causal baroreflex gain estimates were always lower than the corresponding noncausal values and decreased significantly from rest to tilt in both frequency bands. The tilt-induced increase of the phase lag from SAP to RR suggested a shift from vagal to sympathetic modulation. Thus the importance of nonbaroreflex interactions pointed out the necessity of accounting for causality in the cross-spectral analysis of the interactions between cardiovascular variables in healthy humans.

Blood Pressure and Pulse Rate in the Foetal Sheep

1945 ◽  
Vol 22 (1-2) ◽  
pp. 63-74
Author(s):  
JOSEPH BARCROFT ◽  
D. H. BARRON
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Pulse Rate ◽  
Umbilical Artery ◽  
The Central Nervous System ◽  
The Right ◽  
First Moment ◽  
Left Vagus ◽  
Stimulation Of

1. A method (the needle method) is described for the measurement of the pressure in the stream going through a vessel. 2. In the foetal sheep the needle method applied to the umbilical artery gives substantially the same results as the mercurial manometer applied to the carotid, until about half-way through the gestation period. 3. As gestation proceeds the needle method applied at the first moment at which it can be applied to the umbilical artery (or a branch) gives readings substantially lower, and increasingly lower as gestation proceeds, than does the mercurial manometer read at the first moment at which it can be read. 4. The discrepancy is due to the sum of a number of causes which are discussed, but of these the most important is an actual rise of pressure between the time of delivery and the completion of the dissections contingent on the use of the mercurial manometer. 5. The cause of this is not at present demonstrated, but either or both of two factors may be concerned: (a) a dulling of the central nervous system which weakens the depressor reflex; (b) the establishment of a greater degree of vasomotor tone consequent on the bombardment of the central nervous system with sensory stimuli. 6. The pulse rates in utero and just after delivery of the foetus into a saline bath at 39-40°C. (the umbilical circulation being unimpaired) are not significantly different. 7. The pulse rate quickens up to the 70th-80th day, after which it becomes slower as gestation proceeds. 8. If both vagi be severed, the pulse rate te to quicken throughout gestation. The pulse, therefore, comes increasingly under vagus inhibition from the 80th-90th day onwards. 9. Even after the vagi have been cut after the 120th day (it has not been tried before) adrenalin in sufficient quantity will cause a further quickening of the pulse. 10. The earliest date at which stimulation of the peripheral end of the right vagus was observed to slow the heart was the 77th day. On the 85th day peripheral stimulation of the left vagus also failed, but succeeded on the 101st day. 11. Central stimulation of the left vagus, with the right vagus intact, produced slowing on the 77th day. 12. Slowing of the heart synchronous with rise of arterial pressure has been observed on the 111th day. 13. Slowing of the heart which bears evidence of being reflex has been obtained by raising the blood pressure (clamping the cord) on the 121st day and by injection of adrenalin on the 118th day. 14. Approaching term both the carotid sinus and cardiac depressor mechanisms are functional. 15. Lowering of the blood pressure as the result of stimulation of the central end of the vagus and with both vagi severed can be demonstrated late in gestation.

scholarly journals Missing pieces of the Piezo1/Piezo2 baroreceptor hypothesis: an autonomic perspective

2019 ◽  
Vol 122 (3) ◽  
pp. 1207-1212 ◽  
Author(s):  
Sean D. Stocker ◽  
Alan F. Sved ◽  
Michael C. Andresen
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Arterial Blood Pressure ◽  
Tissue Perfusion ◽  
Cellular Mechanism ◽  
Baroreceptor Function ◽  
Arterial Blood ◽  
The Central Nervous System ◽  
Regulation Of Blood Pressure

Baroreceptors play a pivotal role in the regulation of blood pressure through moment to moment sensing of arterial blood pressure and providing information to the central nervous system to make autonomic adjustments to maintain appropriate tissue perfusion. A recent publication by Zeng and colleagues (Zeng WZ, Marshall KL, Min S, Daou I, Chapleau MW, Abboud FM, Liberles SD, Science 362: 464–467, 2018) suggests the mechanosensitive ion channels Piezo1 and Piezo2 represent the cellular mechanism by which baroreceptor nerve endings sense changes in arterial blood pressure. However, before Piezo1 and Piezo2 are accepted as the sensor of baroreceptors, the question must be asked of what criteria are necessary to establish this and how well the report of Zeng and colleagues (Zeng WZ, Marshall KL, Min S, Daou I, Chapleau MW, Abboud FM, Liberles SD, Science 362: 464–467, 2018) satisfies these criteria. We briefly review baroreceptor function, outline criteria that a putative neuronal sensor of blood pressure must satisfy, and discuss whether the recent findings of Zeng and colleagues suitably meet these criteria. Despite the provocative hypothesis, there are significant concerns regarding the evidence supporting a role of Piezo1/Piezo2 in arterial baroreceptor function.

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