A new method to identify dynamic transduction properties of aortic baroreceptors

1990 ◽  
Vol 258 (3) ◽  
pp. H887-H895 ◽  
Author(s):  
M. Sugimachi ◽  
T. Imaizumi ◽  
K. Sunagawa ◽  
Y. Hirooka ◽  
K. Todaka ◽  
...  

We identified, in 17 alpha-chloralose-anesthetized rabbits, the dynamic transduction characteristics of the aortic arch baroreceptors using a "white-noise technique." We recorded aortic pressure and aortic depressor nerve activity while perturbing pressure by rapid, intermittent ventricular pacing (400 beats/min). Dividing the cross-power spectrum between nerve activity and pressure by the power spectrum of pressure yielded the transfer function. The gain of the transfer function increased threefold as the frequency increased from 0.005 to 5 Hz, suggesting that the baroreceptors responded primarily to dynamic rather than to static changes in pressure. To quantify the nonlinear properties of baroreceptor transduction, we compared measured instantaneous nerve activity with that linearly predicted. We demonstrated that the major nonlinearity was attributable to "threshold". The overall baroreceptor transduction properties could be represented by a cascade connection of a linear subsystem followed by a nonlinear subsystem with threshold. The white-noise technique made it possible to identify the unbiased linear properties in a nonlinear system, and thus was very useful in identifying complex biological systems.

1993 ◽  
Vol 264 (3) ◽  
pp. H872-H880 ◽  
Author(s):  
T. Imaizumi ◽  
M. Sugimachi ◽  
Y. Harasawa ◽  
S. Ando ◽  
K. Sunagawa ◽  
...  

To examine the contribution of wall mechanics to dynamic properties of baroreceptors, we subdivided the transfer function of baroreceptors into two subsystems [aortic pressure to diameter and diameter to aortic depressor nerve activity (ANA)]. In six alpha-chloralose-anesthetized rabbits, we measured pressure, diameter, and ANA while randomly perturbing pressure. We obtained transfer functions (pressure to ANA, diameter to ANA, and pressure to diameter) by taking the ratio of crosspower spectrum to the input power spectrum (0.005–5 Hz). Below 3 Hz, the transfer function from pressure to ANA was nearly identical to that from diameter to ANA, whereas that from pressure to diameter was flat. Using transfer functions we could reproduce adaptation and hysteresis that were quantitatively similar between pressure-ANA transduction and diameter-ANA transduction. The pressure-diameter relationship was almost instantaneous and thus showed no hysteresis. In a second group of rabbits, the ratio of the shift of the hysteresis loop was unchanged by ouabain (40 micrograms/kg iv, n = 7). We conclude that the dynamic properties of baroreceptors may not be related to the wall mechanics or the Na(+)-K(+)-adenosinetriphosphatase activity.


1998 ◽  
Vol 274 (1) ◽  
pp. H358-H365 ◽  
Author(s):  
Takayuki Sato ◽  
Toru Kawada ◽  
Toshiaki Shishido ◽  
Hiroshi Miyano ◽  
Masashi Inagaki ◽  
...  

We developed a new method for isolating in situ baroreceptor regions of the rabbit aortic depressor nerve (ADN) and estimated the transfer function from pressure to afferent nerve activity in the frequency range of 0.01–5 Hz by a white noise technique. Complete isolation of the baroreceptor area of the right ADN was made in situ by ligation of the innominate artery and the right subclavian and common carotid arteries. We altered the pressure in the isolated baroreceptor area according to a binary quasi-white noise between 80 and 100 mmHg in 12 urethan-anesthetized rabbits. The gain increased two to three times as the frequency of pressure perturbation increased from 0.01 to 2 Hz and then decreased at higher frequencies. The phase slightly led below 0.2 Hz. The squared coherence value was >0.8 in the frequency range of 0.01–4 Hz. The step responses estimated from the transfer function were indistinguishable from those actually observed. We conclude that the baroreceptor transduction of the ADN is governed by linear dynamics under the physiological operating pressure range.


1994 ◽  
Vol 267 (1) ◽  
pp. H92-H99 ◽  
Author(s):  
H. Masaki ◽  
T. Imaizumi ◽  
Y. Harasawa ◽  
A. Takeshita

Excessive sympathetic nerve activity in heart failure could be attributable to impaired arterial baroreflex function. Employing transfer function analysis, we evaluated the arterial baroreflex in control rabbits (n = 8) and in rabbits with rapid pacing-induced heart failure (n = 10) in a dynamic manner. Rabbits in the heart-failure group showed elevated filling pressures, depressed first derivative of left ventricular pressure, pulmonary congestion, and an increased level of plasma norepinephrine. Varying aortic pressure pseudorandomly and recording responses in renal nerve activity, we calculated the transfer function from aortic pressure to renal nerve activity. The gain of the transfer function was similar between control and heart-failure rabbits over 0.04–0.4 Hz as well as the phase and the coherence, indicating that the dynamic arterial baroreflex was preserved in our rabbit heart-failure model. Vagotomy increased the gain of the arterial baroreflex over 0.04–0.4 Hz in control (P < 0.05) but not in heart-failure rabbits, indicating that vagal afferents, which normally inhibit the dynamic arterial baroreflex, no more did so in heart failure. We conclude that excessive sympathetic nerve activity in heart failure may not be due to impaired dynamic arterial baroreflex, but that this apparently preserved arterial baroreflex in heart failure may be due to impaired cardiopulmonary baroreflex.


1998 ◽  
Vol 275 (2) ◽  
pp. R541-R547 ◽  
Author(s):  
Tsutomu Nakahara ◽  
Toru Kawada ◽  
Masaru Sugimachi ◽  
Hiroshi Miyano ◽  
Takayuki Sato ◽  
...  

Recent investigations in our laboratory using a Gaussian white noise technique showed that the transfer function representing the dynamic properties of transduction from vagus nerve activity to heart rate had characteristics of a first-order low-pass filter. However, the physiological determinants of those characteristics remain to be elucidated. In this study, we stimulated the vagus nerve according to a Gaussian white noise pattern to estimate the transfer function from vagal stimulation to the heart rate response in anesthetized rabbits and examined how changes in acetylcholine kinetics affected the transfer function. We found that although increases in the mean frequency of vagal stimulation from 5 to 10 Hz did not change the characteristics of the transfer function, administration of neostigmine (30 μg ⋅ kg−1 ⋅ h−1iv), a cholinesterase inhibitor, increased the dynamic gain from 8.19 ± 3.66 to 11.7 ± 4.88 beats ⋅ min−1 ⋅ Hz−1( P < 0.05), decreased the corner frequency from 0.12 ± 0.05 to 0.04 ± 0.01 Hz ( P < 0.01), and increased the lag time from 0.17 ± 0.12 to 0.27 ± 0.08 s ( P < 0.05). These results suggest that the rate of acetylcholine degradation at the neuroeffector junction, rather than the amount of available acetylcholine, plays a key role in determining the dynamic properties of transduction from vagus nerve activity to heart rate.


1996 ◽  
Vol 271 (5) ◽  
pp. R1264-R1269 ◽  
Author(s):  
D. E. Claassen ◽  
D. A. Morgan ◽  
T. Hirai ◽  
M. J. Kenney

We tested the hypothesis that sustained increases in mean arterial pressure (MAP) produce nonuniform changes in regional sympathetic nerve discharges (SND) after the return of MAP to control levels. Renal, adrenal, splanchnic, and lumbar SND were recorded before, during, and after a 30-min elevation in MAP produced by phenylephrine (PE) infusion in alpha-chloralose-anesthetized spontaneously hypertensive (SH) rats. SND remained reduced from control values after PE infusion, despite the return of MAP to control levels. Importantly, the duration of poststimulus sympathoinhibition was significantly less in adrenal and splanchnic SND compared with renal and lumbar SND. In sinoaortic-denervated SH rats, SND remained at control levels during and after PE infusion. Simultaneous recordings of aortic depressor nerve (ADN) activity and SND demonstrated that prolonged renal and lumbar sympathoinhibition occurred even when ADN activity fell below control levels after PE infusion. We conclude that poststimulus responses of efferent SND in SH rats are regionally nonuniform and that renal and lumbar sympathoinhibitory responses are not mediated solely by prolonged increases in afferent baroreceptor nerve activity.


1994 ◽  
Vol 266 (1) ◽  
pp. H36-H42 ◽  
Author(s):  
T. Imaizumi ◽  
Y. Harasawa ◽  
S. Ando ◽  
M. Sugimachi ◽  
A. Takeshita

In vagotomized and anesthetized rabbits, aortic pressure (AP), aortic depressor nerve activity (ANA), and renal sympathetic nerve activity (RNA) were simultaneously measured while perturbing AP randomly. To quantitatively characterize the role of the arterial baroreflex system in generating RNA, we determined the transfer function (TF) of the central baroreflex arc from ANA to RNA in the frequency domain (0.02–5 Hz). The magnitude of squared coherence was > 0.5, the phase was close to -180 degrees, and the gain of TF was flat over 0.02–0.3 Hz, indicating that changes in RNA were linearly and instantaneously but inversely related to changes in ANA over this frequency range. Above 0.3 Hz, the coherence was low, suggesting that RNA unrelated to ANA existed in the frequency range. In animals without AP perturbations, power spectrum of RNA resided over 0.2–5 Hz with a broad peak at 1 Hz, which may represent central activity. Our results suggest that over 0.02–0.3 Hz the relationship between arterial baroreceptor afferent nerve activity and RNA is linear and instantaneous but above 0.3 Hz it is not linear possibly due to an interaction between central activity and arterial baroreflex.


1997 ◽  
Vol 273 (1) ◽  
pp. H38-H43 ◽  
Author(s):  
H. Miyano ◽  
T. Kawada ◽  
M. Sugimachi ◽  
T. Shishido ◽  
T. Sato ◽  
...  

We examined whether the inhibition of nitric oxide (NO) synthesis potentiates the dynamic sympathetic regulation of the cardiovascular system through the baroreflex. In anesthetized rabbits, we imposed random pressure perturbations on the isolated carotid sinuses to evoke random changes in sympathetic nerve activity (SNA). We estimated the transfer functions from SNA to both aortic pressure (AoP) and heart rate (HR). The inhibition of NO synthesis by NG-monomethyl-L-arginine (L-NMMA, 40 mg/ kg) altered neither the transfer function from SNA to AoP nor that from SNA to HR. In contrast, sodium nitroprusside (3-6 micrograms.kg-1.min-1) significantly decreased the steady-state gain (40.3 +/- 11.7% of the control, P < 0.05) of the transfer function from SNA to AoP without affecting the HR responses. We conclude that the basal release of NO may have a role in the tonic blood pressure regulation, whereas it may not be involved in the dynamic sympathetic regulation of AoP or HR through the baroreflex.


1991 ◽  
Vol 260 (6) ◽  
pp. H1760-H1766 ◽  
Author(s):  
Y. Hirooka ◽  
S. Ando ◽  
T. Imaizumi ◽  
S. Suzuki ◽  
A. Takeshita

It has been shown that prostacyclin (PGI2) sensitizes cardiac receptors. However, the effects of PGI2 on arterial baroreceptors are not well understood. In rabbits anesthetized with alpha-chloralose (n = 12), we examined reflex changes in multiunit efferent renal sympathetic nerve activity (RSNA) during hypotension caused by intravenous PGI2 (0.1, 0.2, 0.5, 1.0, 2.0 micrograms/kg), nitroglycerin (NG; 5, 10, 20, 50, 100 micrograms/kg), and sodium nitroprusside (SNP; 5, 10, 20, 50, 100 micrograms/kg) before and after bilateral vagotomy. Before vagotomy, RSNA increased during hypotension caused by NG or SNP (P less than 0.01) but did not significantly change during comparable hypotension caused by PGI2. After vagotomy, PGI2 increased RSNA as much as NG or SNP. In another group (n = 6), we examined the changes in aortic pressure (AoP), multiunit afferent aortic nerve activity (ANA), and the aortic diameter (AoD) during hypotension caused by intravenous PGI2, NG, and SNP. The relationship between changes in AoP and those in ANA did not differ during hypotension caused by the three drugs. The relationship between changes in AoP and those in AoD and that between changes in AoD and those in ANA also did not differ. Finally, we examined changes in AoP, ANA, and AoD during ramp increases or decreases of AoP caused by intravenous angiotensin II or NG under background infusion of saline, PGI2, or SNP (n = 6). The relationship among these variables did not differ during infusion of PGI2 and SNP. These results suggest that PGI2 stimulates cardiac receptors with vagal afferents but does not sensitize arterial baroreceptors.


2011 ◽  
Vol 279 ◽  
pp. 361-366
Author(s):  
Quan Yuan ◽  
Yan Shen ◽  
Liang Chen

Stochastic resonance (SR) is a nonlinear phenomenon which can be used to detect weak signal. The theory of SR in a biased mono-stable system driven by multiplicative and additive white noise as well as a weak periodic signal is investigated. The virtual instrument (VI) for weak signal detecting based on this theory is designed with LabVIEW. This instrument can be used to detect weak periodic signals which meets the conditions given and can greatly improved the power spectrum of the weak signal. The results that related to different sets of parameters are given and the features of these results are in accordance with the theory of mono-stable SR. Thus, the application of this theory in the detecting of weak signal is proven to be valid.


1980 ◽  
Vol 239 (1) ◽  
pp. R137-R142 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu

To investigate the role of the paraventricular (PAH) and supraoptic (SON) nuclei in regulation of the cardiovascular system experiments were done in 26 cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. Electrical stimulation of histologically verified sites in the region of the PAH and SON elicited increases in arterial pressure in bilaterally vagotomized animals and increases in heart rate both in spinal (C2) animals and in animals bilaterally vagotomized, In addition, stimulation of either the PAH or SON inhibited the reflex vagal bradycardia elicited by stimulation of the carotid sinus nerve (CSN) and bilateral lesions of these areas increased the magnitude of the response. On the other hand, stimulation and lesions of these hypothalamic regions did not alter the magnitude of the cardiovascular responses to stimulation of the aortic depressor nerve. These results demonstrate that stimulation of the PAH and SON elicit cardiovascular responses due to reciprocal changes in activity of the parasympathetic and sympathetic nervous systems and that these structures maintain a tonic inhibitory influence on the heart rate component of the CSN reflex.


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