Effects of neuronal norepinephrine uptake blockade on baroreflex neural and peripheral arc transfer characteristics

2004 ◽  
Vol 286 (6) ◽  
pp. R1110-R1120 ◽  
Author(s):  
Toru Kawada ◽  
Tadayoshi Miyamoto ◽  
Kazunori Uemura ◽  
Koji Kashihara ◽  
Atsunori Kamiya ◽  
...  
Keyword(s):  
Transfer Function ◽  
Sympathetic Nerve ◽  
Neuronal Uptake ◽  
Arterial Baroreflex ◽  
Exogenous Disturbance ◽  
Sympathetic Regulation ◽  
White Noise Sequence ◽  
Noise Sequence ◽  
Normalized Gain ◽  
Sinus Pressure

Neuronal uptake is the most important mechanism by which norepinephrine (NE) is removed from the synaptic clefts at sympathetic nerve terminals. We examined the effects of neuronal NE uptake blockade on the dynamic sympathetic regulation of the arterial baroreflex because dynamic characteristics are important for understanding the system behavior in response to exogenous disturbance. We perturbed intracarotid sinus pressure (CSP) according to a binary white noise sequence in anesthetized rabbits, while recording cardiac sympathetic nerve activity (SNA), arterial pressure (AP), and heart rate (HR). Intravenous administration of desipramine (1 mg/kg) decreased the normalized gain of the neural arc transfer function from CSP to SNA relative to untreated control (1.03 ± 0.09 vs. 0.60 ± 0.08 AU/mmHg, mean ± SE, P < 0.01) but did not affect that of the peripheral arc transfer function from SNA to AP (1.10 ± 0.05 vs. 1.08 ± 0.10 mmHg/AU). The normalized gain of the transfer function from SNA to HR was unaffected (1.01 ± 0.04 vs. 1.09 ± 0.12 beats·min−1·AU−1). Desipramine decreased the natural frequency of the transfer function from SNA to AP by 28.7 ± 7.0% (0.046 ± 0.007 vs. 0.031 ± 0.002 Hz, P < 0.05) and that of the transfer function from SNA to HR by 64.4 ± 2.2% (0.071 ± 0.003 vs. 0.025 ± 0.002 Hz, P < 0.01). In conclusion, neuronal NE uptake blockade by intravenous desipramine administration reduced the total buffering capacity of the arterial baroreflex mainly through its action on the neural arc. The differential effects of neuronal NE uptake blockade on the dynamic AP and HR responses to SNA may provide clues for understanding the complex pathophysiology of cardiovascular diseases associated with neuronal NE uptake deficiency.

Dynamic arterial baroreflex in rabbits with heart failure induced by rapid pacing

1994 ◽  
Vol 267 (1) ◽  
pp. H92-H99 ◽  
Author(s):  
H. Masaki ◽  
T. Imaizumi ◽  
Y. Harasawa ◽  
A. Takeshita
Keyword(s):  
Heart Failure ◽  
Transfer Function ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Aortic Pressure ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Rapid Pacing

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.

Bezold-Jarisch reflex attenuates dynamic gain of baroreflex neural arc

2003 ◽  
Vol 285 (2) ◽  
pp. H833-H840 ◽  
Author(s):  
Koji Kashihara ◽  
Toru Kawada ◽  
Yusuke Yanagiya ◽  
Kazunori Uemura ◽  
Masashi Inagaki ◽  
...  
Keyword(s):  
Transfer Function ◽  
Myocardial Ischemia ◽  
Dynamic Characteristics ◽  
Acute Myocardial Ischemia ◽  
Renal Sympathetic Nerve Activity ◽  
Afferent Nerves ◽  
Before And After ◽  
White Noise Sequence ◽  
Noise Sequence ◽  
Dynamic Gain

Although acute myocardial ischemia or infarction may induce the Bezold-Jarisch (BJ) reflex through the activation of serotonin receptors on vagal afferent nerves, the mechanism by which the BJ reflex modulates the dynamic characteristics of arterial pressure (AP) regulation is unknown. The purpose of this study was to examine the effects of the BJ reflex induced by intravenous phenylbiguanide (PBG) on the dynamic characteristics of the arterial baroreflex. In seven anesthetized rabbits, we perturbed intracarotid sinus pressure (CSP) according to a white noise sequence while renal sympathetic nerve activity (RSNA), AP, and heart rate (HR) were recorded. We estimated the transfer function from CSP to RSNA (neural arc) and from RSNA to AP (peripheral arc) before and after 10 min of intravenous administration of PBG (100 μg · kg–1 · min–1). The intravenous PBG decreased mean AP from 84.5 ± 4.0 to 68.2 ± 4.7 mmHg ( P < 0.01), mean RSNA to 76.2 ± 7.0% ( P < 0.05), and mean HR from 301.6 ± 7.7 to 288.4 ± 9.0 beats/min ( P < 0.01). The intravenous PBG significantly decreased neural arc dynamic gain at 0.01 Hz (1.06 ± 0.08 vs. 0.59 ± 0.17, P < 0.05), whereas it did not affect that of the peripheral arc (1.20 ± 0.12 vs. 1.18 ± 0.41). In six different rabbits without intravenous PBG, the neural arc transfer function did not change between two experimental runs with intervening interval of 10 min, excluding the possibility that the cumulative effects of anesthetics had altered the neural arc transfer function. In conclusion, excessive activation of the BJ reflex during acute myocardial ischemia may exert an adverse effect on AP regulation, not only by sympathetic suppression, but also by attenuating baroreflex dynamic gain.

Static interaction between muscle mechanoreflex and arterial baroreflex in determining efferent sympathetic nerve activity

2005 ◽  
Vol 289 (4) ◽  
pp. H1604-H1609 ◽  
Author(s):  
Kenta Yamamoto ◽  
Toru Kawada ◽  
Atsunori Kamiya ◽  
Hiroshi Takaki ◽  
Masaru Sugimachi ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Tension ◽  
Open Loop ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Parallel Shift ◽  
Response Range ◽  
Sympathetic Regulation ◽  
Muscle Mechanoreflex

Elucidation of the interaction between the muscle mechanoreflex and the arterial baroreflex is essential for better understanding of sympathetic regulation during exercise. We characterized the effects of these two reflexes on sympathetic nerve activity (SNA) in anesthetized rabbits ( n = 7). Under open-loop baroreflex conditions, we recorded renal SNA at carotid sinus pressure (CSP) of 40, 80, 120, or 160 mmHg while passively stretching the hindlimb muscle at muscle tension (MT) of 0, 2, 4, or 6 kg. The MT-SNA relationship at CSP of 40 mmHg approximated a straight line. Increase in CSP from 40 to 120 and 160 mmHg shifted the MT-SNA relationship downward and reduced the response range (the difference between maximum and minimum SNA) to 43 ± 10% and 19 ± 6%, respectively ( P < 0.01). The CSP-SNA relationship at MT of 0 kg approximated a sigmoid curve. Increase in MT from 0 to 2, 4, and 6 kg shifted the CSP-SNA relationship upward and extended the response range to 133 ± 8%, 156 ± 14%, and 178 ± 15%, respectively ( P < 0.01). A model of algebraic summation, i.e., parallel shift, with a threshold of SNA functionally reproduced the interaction of the two reflexes ( y = 1.00 x − 0.01; r2 = 0.991, root mean square = 2.6% between estimated and measured SNA). In conclusion, the response ranges of SNA to baroreceptor and muscle mechanoreceptor input changed in a manner that could be explained by a parallel shift with threshold.

Arterial baroreflex control of cardiac and renal sympathetic nerve activities is uniform in frequency domain

1991 ◽  
Vol 261 (2) ◽  
pp. R296-R300 ◽  
Author(s):  
S. Harada ◽  
S. Ando ◽  
T. Imaizumi ◽  
Y. Hirooka ◽  
K. Sunagawa ◽  
...  
Keyword(s):  
Phase Shift ◽  
Transfer Function ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Arterial Baroreflex ◽  
Frequency Range ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

To investigate wideband dynamic properties of arterial baroreflex control of cardiac and renal sympathetic nerve activities, we assessed the transfer function using a "white-noise technique." In pentobarbital sodium-anesthetized cats, we simultaneously recorded, as the output, cardiac sympathetic nerve activity (CSNA) and renal sympathetic nerve activity (RSNA), while aortic pressure (AP) was randomly perturbed to impose input pressure changes with broad frequencies. We calculated the transfer function from AP to CSNA or to RSNA over the frequency range of 0.01-5 Hz through the spectral analysis of the input and output. We found that the gain, phase shift, and coherence of those transfer functions were statistically indistinguishable. The gain was rather flat below 0.05 Hz, steadily increased above 0.05 Hz, and plateaued above 0.3 Hz. The phase shift was out of phase up to 0.05 Hz and led by approximately 4 degrees above 0.05 Hz. The coherence was high (above 0.7) below 0.3 Hz and became lower above 0.3 Hz. These results suggest that arterial baroreflex control is uniform and similar between the two activities in the frequency range of 0.01-0.7 Hz.

Inhibition of NO synthesis does not potentiate dynamic cardiovascular response to sympathetic nerve activity

1997 ◽  
Vol 273 (1) ◽  
pp. H38-H43 ◽  
Author(s):  
H. Miyano ◽  
T. Kawada ◽  
M. Sugimachi ◽  
T. Shishido ◽  
T. Sato ◽  
...  
Keyword(s):  
Transfer Function ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Transfer Functions ◽  
Cardiovascular Response ◽  
Aortic Pressure ◽  
Nerve Activity ◽  
Basal Release ◽  
Sympathetic Regulation ◽  
Pressure Perturbations

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.

Parallel resetting of arterial baroreflex control of renal and cardiac sympathetic nerve activities during upright tilt in rabbits

2010 ◽  
Vol 298 (6) ◽  
pp. H1966-H1975 ◽  
Author(s):  
Atsunori Kamiya ◽  
Toru Kawada ◽  
Masaki Mizuno ◽  
Shuji Shimizu ◽  
Masaru Sugimachi
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Response Range ◽  
Sigmoidal Curve ◽  
Maximal Gain ◽  
Upright Tilt ◽  
Sinus Pressure

Since humans are under ceaseless orthostatic stress, the mechanisms to maintain arterial pressure (AP) against gravitational fluid shift are important. As one mechanism, it was reported that upright tilt reset baroreflex control of renal sympathetic nerve activity (SNA) to a higher SNA in anesthetized rabbits. In the present study, we tested the hypothesis that upright tilt causes a parallel resetting of baroreflex control of renal and cardiac SNAs in anesthetized rabbits. In anesthetized rabbits ( n = 8, vagotomized and aortic denervated) with 0° supine and 60° upright tilt postures, renal and cardiac SNAs were simultaneously recorded while isolated intracarotid sinus pressure (CSP) was increased stepwise from 40 to 160 mmHg with increments of 20 mmHg. Upright tilt shifted the reverse-sigmoidal curve of the CSP-SNA relationship to higher SNA similarly in renal and cardiac SNAs. Although upright tilt increased the maximal gain, the response range and the minimum value of SNA, the curves were almost superimposable in these SNAs regardless of postures. Scatter plotting of cardiac SNA over renal SNA during the stepwise changes in CSP was close to the line of identity in 0° supine and 60° upright tilt postures. In addition, upright tilt also shifted the reverse-sigmoidal curve of the CSP-heart rate relationship to a higher heart rate, with increases in the maximal gain and the response range. In conclusion, upright posture caused a resetting of arterial baroreflex control of SNA similarly in renal and cardiac SNAs in anesthetized rabbits.

Arterial baroreflex dynamics in normotensive and spontaneously hypertensive rats

1992 ◽  
Vol 263 (3) ◽  
pp. R524-R528 ◽  
Author(s):  
S. Harada ◽  
T. Imaizumi ◽  
S. Ando ◽  
Y. Hirooka ◽  
K. Sunagawa ◽  
...  
Keyword(s):  
Transfer Function ◽  
Sympathetic Nerve ◽  
Spontaneously Hypertensive Rats ◽  
Sympathetic Nerve Activity ◽  
Arterial Baroreflex ◽  
Frequency Range ◽  
Hypertensive Rats ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Spontaneously Hypertensive

To investigate dynamic or frequency-dependent characteristics of arterial baroreflex control of efferent sympathetic nerve activity in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY), we assessed the transfer function from aortic pressure (AP) to renal sympathetic nerve activity (RSNA) using a “white-noise technique.” In pentobarbital sodium-anesthetized rats, we recorded RSNA as the output, while AP was randomly perturbed to impose input pressure changes with broad frequencies. We calculated the transfer function from AP to RSNA over the frequency range of 0.01-5 Hz through the spectral analysis of the input and output. The results indicated that the gain, phase shift, and coherence of the transfer function for SHR and for WKY were similar and statistically indistinguishable. The gain was relatively constant below 0.05 Hz but increased steadily by fivefold as frequency increased in the frequency range of 0.05-0.8 Hz. The phase was out of phase where coherence was high. The coherence was high (greater than 0.5) in the frequency range of 0.04-0.8 and 1.00-1.03 Hz but was low in other frequencies. These results suggest that dynamic or frequency-dependent characteristics of arterial baroreflex control of RSNA were not altered in SHR as compared with WKY.

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