Low Pressure Baroreflex Evokes Biphasic Change in Sympathetic Nerve Activity through Vagal Nerve

2013 ◽  
Vol 19 (10) ◽  
pp. S161
Author(s):  
Yasuhiro Oga ◽  
Takuya Kishi ◽  
Keita Saku ◽  
Takamori Kakino ◽  
Masataka Ikeda ◽  
...  
2005 ◽  
Vol 289 (4) ◽  
pp. H1758-H1769 ◽  
Author(s):  
Atsunori Kamiya ◽  
Junichiro Hayano ◽  
Toru Kawada ◽  
Daisaku Michikami ◽  
Kenta Yamamoto ◽  
...  

Sympathetic activation during orthostatic stress is accompanied by a marked increase in low-frequency (LF, ∼0.1-Hz) oscillation of sympathetic nerve activity (SNA) when arterial pressure (AP) is well maintained. However, LF oscillation of SNA during development of orthostatic neurally mediated syncope remains unknown. Ten healthy subjects who developed head-up tilt (HUT)-induced syncope and 10 age-matched nonsyncopal controls were studied. Nonstationary time-dependent changes in calf muscle SNA (MSNA, microneurography), R-R interval, and AP (finger photoplethysmography) variability during a 15-min 60° HUT test were assessed using complex demodulation. In both groups, HUT during the first 5 min increased heart rate, magnitude of MSNA, LF and respiratory high-frequency (HF) amplitudes of MSNA variability, and LF and HF amplitudes of AP variability but decreased HF amplitude of R-R interval variability (index of cardiac vagal nerve activity). In the nonsyncopal group, these changes were sustained throughout HUT. In the syncopal group, systolic AP decreased from 100 to 60 s before onset of syncope; LF amplitude of MSNA variability decreased, whereas magnitude of MSNA and LF amplitude of AP variability remained elevated. From 60 s before onset of syncope, MSNA and heart rate decreased, index of cardiac vagal nerve activity increased, and AP further decreased to the level at syncope. LF oscillation of MSNA variability decreased during development of orthostatic neurally mediated syncope, preceding sympathetic withdrawal, bradycardia, and severe hypotension, to the level at syncope.


2014 ◽  
Vol 2 (9) ◽  
pp. e12136 ◽  
Author(s):  
Keita Saku ◽  
Takuya Kishi ◽  
Kazuo Sakamoto ◽  
Kazuya Hosokawa ◽  
Takafumi Sakamoto ◽  
...  

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Yasuhiro Oga ◽  
Takuya Kishi ◽  
Keita Saku ◽  
Takamori Kakino ◽  
Akiko Nishizaki ◽  
...  

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Keita Saku ◽  
Kazuo Sakamoto ◽  
Kazuya Hosokawa ◽  
Takamori Kakino ◽  
Masataka Ikeda ◽  
...  

2019 ◽  
Vol 317 (2) ◽  
pp. R337-R345 ◽  
Author(s):  
Yuhichi Kuda ◽  
Mamoru Tanida ◽  
Fu Chen ◽  
Yasutaka Kurata ◽  
Toshishige Shibamoto

Systemic anaphylaxis is a life-threatening and allergic reaction that affects various organs. We previously reported that, in the stomach, gastric vasoconstriction occurring at the late phase (15–55 min after injection of ovalbumin antigen) was observed in anesthetized rats sensitized with ovalbumin. In addition, anaphylaxis enhances gastric motility and delays emptying. However, the role of extrinsic autonomic nervous system on antigen-induced gastric alterations was not known. Thus, using the same rat anaphylaxis model, we aimed to determine the changes in the efferent and afferent autonomic nerve activities in the stomach during anaphylactic hypotension. The findings showed that injection of ovalbumin antigen caused substantial systemic hypotension in all sensitized rats. The efferent gastric sympathetic nerve activity (ef-GSNA), but not the efferent vagal nerve activity, increased only at the early phase (1–10 min after injection of ovalbumin antigen) and showed baroreceptor reflex, as evidenced by a stimulatory response to sodium nitroprusside-induced hypotension. In general, excitation of ef-GSNA could induce pylorus sphincter contraction and gastric vasoconstriction. In the present study, we found that sympathectomy attenuated the anaphylaxis-induced decrease in gastric flux but not the increase in gastric vascular resistance. Thus, the increase in ef-GSNA may cause anaphylactic pylorus sphincter contraction but not anaphylactic gastric vasoconstriction. On the other hand, the afferent gastric vagal nerve activity, but not the afferent sympathetic nerve activity, increased during the early phase of anaphylactic hypotension. However, vagotomy produced no effects on the anaphylactic gastric dysfunction. In conclusion, the gastric sympathetic nerves partly modulate stomach function during systemic anaphylaxis.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yasuhiro Oga ◽  
Takuya Kishi ◽  
Keita Saku ◽  
Takamori Kakino ◽  
Akiko Nishizaki ◽  
...  

Background: Arterial baroreflex is a powerful regulator of the sympathetic nerve activity (SNA) and arterial pressure (AP). Although vagal nerve stimulation (VNS) has been developed as a neuro-modulatory therapy for heart failure, the impact of VNS on baroreflex and SNA remains unknown. Since the afferent fibers of vagal nerves and of baroreceptors converge in the nucleus tractus solitarii, we investigated how the selective afferent VNS (AVNS) impacts on baroreflex in regulating SNA and AP. Methods: We used 6 anesthetized Sprague-Dawley rats (530±11g). We vascularly isolated bilateral carotid sinuses and servo-controlled intra-sinus pressure (CSP). We measured AP, CSP and splanchnic SNA simultaneously. We attached an electrode to the vagal nerve. We established the baseline intensity (voltage) of VNS that reduced heart rate by 10-20%. We then sectioned the vagal nerve at the caudal side of the electrode. We conducted AVNS at 3 doses, baseline, 2xbaseline and 4xbaseline. We changed CSP stepwise from 60 to 160mmHg to analyze static baroreflex function with/without AVNS. To estimate dynamic baroreflex function, we perturbed CSP using binary random sequence (mean AP±20mmHg) and compared the transfer functions (TF) with/without AVNS. Results: AVNS dose-dependently shifted the CSP-SNA relation downward (p<0.05, Fig. 1) without changing the maximum gain, while did not affect the SNA-AP relation (Fig. 2). The TF of CSP-SNA relation approximated a high pass filter characteristics. AVNS dose-dependently decreased the dynamic gain (Control: 0.72±0.20, baseline: 0.46±0.14, 2xbaseline: 0.38±0.12, 4xbaseline: 0.20±0.08 %/mmHg, p<0.05), whereas did not affect the TF of SNA-AP relation. Conclusions: AVNS dose-dependently suppresses SNA by resetting the static CSP-SNA relation, i.e., the baroreflex central arc. However, AVNS reduces the dynamic gain of baroreflex central arc. We conclude that AVNS lowers SNA at the expense of compromising dynamic AP stabilization.


1987 ◽  
Vol 253 (1) ◽  
pp. H133-H137 ◽  
Author(s):  
P. Thoren ◽  
D. A. Morgan ◽  
A. L. Mark

Vagal afferent pathways contribute to vasomotor inhibition and renal sodium handling by modulating sympathetic nerve activity in rats. Low pressure or cardiopulmonary baroreflex inhibition of sympathetic nerve activity is attenuated in normotensive Dahl salt-sensitive (S) rats fed a low-salt diet. The aim of the study was to record activity in single-fiber vagal filaments from left atrial endings in Dahl S and resistant (R) rats to evaluate the mechanism for the attenuated low pressure baroreflex. Rats were fed a low-salt diet (0.1% NaCl) for 5–7 wk. Seven Dahl R and six S rats were anesthetized with urethan, and catheters were placed in the aorta and left atrium. Single-fiber recordings were obtained from the right cervical vagus. The relationship between left atrial pressure and receptor discharge was obtained during graded aortic snaring. Mean threshold for increased activation of the vagal afferents during volume expansion was 10.4 +/- 0.6 mmHg (means +/- SE) in S and 6.0 +/- 0.4 mmHg in R rats (P less than 0.002). Pressure-discharge curves were significantly shifted to the right in S rats. Maximal sensitivity of the endings expressed as delta discharge/delta LAP was not significantly different in R vs. S, but the right shift in threshold reduced the discharge of endings over a physiological range of filling pressures. We also measured left ventricular end-diastolic pressure (LVEDP) in conscious S and R rats to determine if the resetting of left atrial sensory endings could be explained by elevated left heart filling pressure.(ABSTRACT TRUNCATED AT 250 WORDS)


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