Dynamic interactions between arterial pressure and sympathetic nerve activity: role of arterial baroreceptors

2003 ◽  
Vol 285 (4) ◽  
pp. R834-R841 ◽  
Author(s):  
Claude Julien ◽  
Bruno Chapuis ◽  
Yong Cheng ◽  
Christian Barrès
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Noise Sources ◽  
Nerve Activity ◽  
Pass Filter ◽  
Low Pass Filter ◽  
Mayer Waves ◽  
Arterial Baroreceptors

The role of arterial baroreceptors in controlling arterial pressure (AP) variability through changes in sympathetic nerve activity was examined in conscious rats. AP and renal sympathetic nerve activity (RSNA) were measured continuously during 1-h periods in freely behaving rats that had been subjected to sinoaortic baroreceptor denervation (SAD) or a sham operation 2 wk before study ( n = 10 in each group). Fast Fourier transform analysis revealed that chronic SAD did not alter high-frequency (0.75-5 Hz) respiratory-related oscillations of mean AP (MAP) and RSNA, decreased by ∼50% spectral power of both variables in the midfrequency band (MF, 0.27-0.74 Hz) containing the so-called Mayer waves, and induced an eightfold increase in MAP power without altering RSNA power in the low-frequency band (0.005-0.27 Hz). In both groups of rats, coherence between RSNA and MAP was maximal in the MF band and was usually weak at lower frequencies. In SAD rats, the transfer function from RSNA to MAP showed the characteristics of a second-order low-pass filter containing a fixed time delay (∼0.5 s). These results indicate that arterial baroreceptors are not involved in production of respiratory-related oscillations of RSNA but play a major role in the genesis of synchronous oscillations of MAP and RSNA at the frequency of Mayer waves. The weak coupling between slow fluctuations of RSNA and MAP in sham-operated and SAD rats points to the interference of noise sources unrelated to RSNA affecting MAP and of noise sources unrelated to MAP affecting RSNA.

scholarly journals Dynamic relationship between sympathetic nerve activity and renal blood flow: a frequency domain approach

2001 ◽  
Vol 281 (1) ◽  
pp. R206-R212 ◽  
Author(s):  
Sarah-Jane Guild ◽  
Paul C. Austin ◽  
Michael Navakatikyan ◽  
John V. Ringwood ◽  
Simon C. Malpas
Keyword(s):  
Blood Flow ◽  
Transfer Function ◽  
Renal Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Pass Filter ◽  
Low Pass Filter ◽  
Dynamic Relationship ◽  
Transfer Function Analysis

Blood pressure displays an oscillation at 0.1 Hz in humans that is well established to be due to oscillations in sympathetic nerve activity (SNA). However, the mechanisms that control the strength or frequency of this oscillation are poorly understood. The aim of the present study was to define the dynamic relationship between SNA and the vasculature. The sympathetic nerves to the kidney were electrically stimulated in six pentobarbital-sodium anesthetized rabbits, and the renal blood flow response was recorded. A pseudo-random binary sequence (PRBS) was applied to the renal nerves, which contains equal spectral power at frequencies in the range of interest (<1 Hz). Transfer function analysis revealed a complex system composed of low-pass filter characteristics but also with regions of constant gain. A model was developed that accounted for this relationship composed of a 2 zero/4 pole transfer function. Although the position of the poles and zeros varied among animals, the model structure was consistent. We also found the time delay between the stimulus and the RBF responses to be consistent among animals (mean 672 ± 22 ms). We propose that the identification of the precise relationship between SNA and renal blood flow (RBF) is a fundamental and necessary step toward understanding the interaction between SNA and other physiological mediators of RBF.

Osmolality: a physiological long-term regulator of lumbar sympathetic nerve activity and arterial pressure

1999 ◽  
Vol 276 (6) ◽  
pp. R1579-R1586 ◽  
Author(s):  
Karie E. Scrogin ◽  
Eugene T. Grygielko ◽  
Virginia L. Brooks
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Cumulative Effect ◽  
Physiological Changes ◽  
Progressive Reduction ◽  
Nerve Activity

Acute infusion of hypertonic fluid increases mean arterial pressure (MAP) in part by elevating nonrenal sympathetic activity. However, it is not known whether chronic, physiological increases in osmolality also increase sympathetic activity. To test this hypothesis, MAP, heart rate (HR), and lumbar sympathetic nerve activity (LSNA) were measured in conscious, 48-h water-deprived rats (WD) during a progressive reduction in osmolality produced by a 2-h systemic infusion (0.12 ml/min) of 5% dextrose in water (5DW). Water deprivation significantly increased osmolality (308 ± 2 vs. 290 ± 2 mosmol/kgH2O, P < 0.001), HR (453 ± 7 vs. 421 ± 10 beats/min, P < 0.05), and LSNA (63.5 ± 1.8 vs. 51.9 ± 3.8% baroreflex maximum, P < 0.01). Two hours of 5DW infusion reduced osmolality (−15 ± 5 mosmol/kgH2O), LSNA (−23 ± 3% baseline), and MAP (−10 ± 1 mmHg). To evaluate the role of vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist. The antagonist lowered MAP (−5 ± 1 mmHg) and elevated HR (32 ± 7 beats/min) and LSNA (11 ± 3% baseline) in WD ( P < 0.05), but not in water-replete, rats. 5DW infusion had a similar cumulative effect on all variables in V1-blocked WD rats, but had no effect in water-replete rats. Infusion of the same volume of normal saline in WD rats did not change osmolality, LSNA or MAP. Together these data indicate that, in dehydrated rats, vasopressin supports MAP and suppresses LSNA and HR and that physiological changes in osmolality directly influence sympathetic activity and blood pressure independently of changes in vasopressin and blood volume.

scholarly journals Role of Corticotrophin-Releasing Factor in Effects of Leptin on Sympathetic Nerve Activity and Arterial Pressure

Hypertension ◽  
2001 ◽  
Vol 38 (3) ◽  
pp. 384-388 ◽  
Author(s):  
Marcelo L.G. Correia ◽  
Donald A. Morgan ◽  
Jennifer L. Mitchell ◽  
William I. Sivitz ◽  
Allyn L. Mark ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Corticotrophin Releasing Factor

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

1986 ◽  
Vol 251 (3) ◽  
pp. H644-H655 ◽  
Author(s):  
G. B. Guo ◽  
P. G. Schmid ◽  
F. M. Abboud
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Intravenous Infusion ◽  
Sympathetic Nerve Activity ◽  
Central Action ◽  
Nerve Activity ◽  
Arterial Baroreceptors ◽  
Aortic Depressor Nerve ◽  
Carotid Baroreflex ◽  
Vagal Nerves

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.

Contrasting effects of vasopressin on baroreflex inhibition of lumbar sympathetic nerve activity

1985 ◽  
Vol 249 (5) ◽  
pp. H922-H928 ◽  
Author(s):  
F. M. Sharabi ◽  
G. B. Guo ◽  
F. M. Abboud ◽  
M. D. Thames ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Urinary Osmolality ◽  
Arterial Baroreceptors ◽  
Sprague Dawley Rats ◽  
The Difference ◽  
High Level

Baroreflex inhibition of lumbar sympathetic nerve activity (LSNA) during intravenous infusions of phenylephrine and vasopressin is contrasted in rats and rabbits. In rabbits, vasopressin caused smaller increases in arterial pressure and greater inhibition of LSNA than phenylephrine. In Sprague-Dawley rats, however, both vasopressin and phenylephrine caused equivalent increases in arterial pressure and reflex reductions in LSNA. The inhibition of LSNA was mediated through the arterial baroreceptors in both species because it was abolished by sinoaortic denervation. In rats, the possibility that a high level of endogenous vasopressin may have prevented the demonstration of a facilitated baroreflex with the infusion of exogenous vasopressin is unlikely since vasopressin also did not facilitate the reflex in Brattleboro rats, which lack circulating vasopressin. Further, Sprague-Dawley rats were responsive to exogenous vasopressin since infusion of increasing doses of vasopressin caused significant increases in urinary osmolality as well as progressive increments in arterial pressure. The results indicate that intravenous vasopressin given for a period of 6 min facilitates the reflex inhibition of LSNA mediated through arterial baroreceptors in rabbits, but not in rats. Vasopressin given for a period of up to 45 min to rats also fails to facilitate baroreflexes, emphasizing the difference from rabbits. In rabbits, this facilitation appears to involve a central mechanism.

Differential control of renal and lumbar sympathetic nerve activity during freezing behavior in conscious rats

2010 ◽  
Vol 299 (4) ◽  
pp. R1114-R1120 ◽  
Author(s):  
Misa Yoshimoto ◽  
Keiko Nagata ◽  
Kenju Miki
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiovascular Function ◽  
Freezing Behavior ◽  
Nerve Activity ◽  
Conscious Rats ◽  
Arterial Baroreceptors

The present study was designed to document changes in sympathetic nerve activity and cardiovascular function when conscious rats were challenged with a noise stressor to induce freezing behavior. The potential contribution of the arterial baroreceptors in regulating sympathetic nerve activity and cardiovascular adjustments during the freezing behavior was then examined. Wistar male rats were assigned to sham-operated (SO) and sinoaortic-denervated (SAD) groups and instrumented chronically with electrodes for measurements of renal (RSNA) and lumbar (LSNA) sympathetic nerve activity, electroencephalogram, electromyogram, and electrocardiogram and catheters for measurements of systemic arterial and central venous pressure. Both SO and SAD rats were exposed to 90 dB of white noise for 10 min, causing freezing behavior in both groups. In SO rats, freezing behavior was associated with an immediate and significant ( P < 0.05) increase in RSNA, no changes in LSNA or mean arterial pressure, and a significant ( P < 0.05) decrease in heart rate. SAD attenuated the magnitude of the immediate increase in RSNA and had no influence on the response in LSNA during freezing behavior compared with SO rats. Moreover, in SAD rats, mean arterial pressure increased significantly ( P < 0.05) while heart rate did not change during the freezing behavior. These data indicate that freezing behavior evokes regionally different changes in sympathetic outflows, which may be involved in generating the patterned responses of cardiovascular function to stressful or threatening sensory stimulation. Moreover, it is suggested that the arterial baroreceptors are involved in generating the differential changes in RSNA and LSNA and thus the patterned changes in cardiovascular functions observed during freezing behavior in conscious rats.

Problems, possibilities, and pitfalls in studying the arterial baroreflexes’ influence over long-term control of blood pressure

2005 ◽  
Vol 288 (4) ◽  
pp. R837-R845 ◽  
Author(s):  
Carolyn J. Barrett ◽  
Simon C. Malpas
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Critical Role ◽  
Pressure Control ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
The Many

While there is no disputing the critical role of baroreflexes in buffering rapid changes in arterial pressure, their role in long-term pressure control has become an area of controversy. Recent experiments using novel techniques have challenged the traditional view that arterial baroreflexes are not involved in setting chronic arterial pressure levels. Resetting of the arterial baroreflex, often used as an argument against the arterial baroreflex playing a role in long-term pressure control is rarely complete. The arterial baroreflex is just one of the many neural, hormonal, and intrinsic mechanisms involved in arterial pressure control and while the removal of the arterial baroreflex alone has little effect on mean arterial pressure it is too simplistic to suggest that the baroreflex has no role in long-term pressure control. Renal sympathetic nerve activity appears to be particularly resistant to resetting in response to ANG II-induced hypertension. Given the important role of the kidneys in long-term pressure control, we suggest there is a clear need to develop experimental techniques whereby sympathetic nerve activity to the kidneys and other organs can be monitored over periods of weeks to months.

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