New simple methods for isolating baroreceptor regions  of carotid sinus and aortic depressor nerves in rats

Sato, Takayuki; Kawada, Toru; Mikami, Hiroshi; Shishido, Toshiaki; Inagaki, Masumi; Yoshimura, Ryoichi; Tatewaki, Teiji; Sugimachi, Masaru; Alexander, Joe; Sunagawa, Kenji

doi:10.1152/ajpheart.1999.276.1.h326

Cited by 73 publications

(68 citation statements)

References 15 publications

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“…Carotid sinus baroreceptor regions were isolated bilaterally from the systemic circulation (23,27), and carotid sinus pressure (CSP) was controlled using a servo-controlled piston pump. Heparin sodium (100 U/kg) was given intravenously to prevent blood coagulation.…”

Section: Methodsmentioning

confidence: 99%

“…However, because most in vivo studies are conducted under baroreflex closedloop conditions, changes in SNA inevitably alter AP, and vice versa. To circumvent this problem, the present study employed a framework of open-loop systems analysis using a baroreceptor isolation preparation (23,27). The arterial baroreflex system may be divided into the neural arc subsystem from pressure input to efferent SNA and the peripheral arc subsystem from SNA to AP (8,17,22).…”

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confidence: 99%

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Effects of tempol on baroreflex neural arc versus peripheral arc in normotensive and spontaneously hypertensive rats

Kawada

Sata

Shimizu

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Kawada T, Sata Y, Shimizu S, Turner MJ, Fukumitsu M, Sugimachi M. Effects of tempol on baroreflex neural arc versus peripheral arc in normotensive and spontaneously hypertensive rats. Am J Physiol Regul Integr Comp Physiol 308: R957-R964, 2015. First published March 25, 2015 doi:10.1152/ajpregu.00525.2014.-Although oxidative redox signaling affects arterial pressure (AP) regulation via modulation of vascular tone and sympathetic nerve activity (SNA), it remains unknown which effect plays a dominant role in the determination of AP in vivo. Open-loop systems analysis of the carotid sinus baroreflex was conducted to separately quantify characteristics of the neural arc from baroreceptor pressure input to SNA and the peripheral arc from SNA to AP in normotensive Wistar-Kyoto (WKY; n ϭ 8) and spontaneously hypertensive rats (SHR; n ϭ 8). Responses in SNA and AP to a staircase-wise increase in carotid sinus pressure were examined before and during intravenous administration of the membrane-permeable superoxide dismutase mimetic tempol (30 mg/kg bolus followed by 30 mg·kg Ϫ1 ·h Ϫ1 ). Two-way ANOVA indicated that tempol significantly decreased the response range of SNA (from 89.1 Ϯ 2.4% to 60.7 Ϯ 2.5% in WKY and from 77.5 Ϯ 3.2% to 56.9 Ϯ 7.3% in SHR, P Ͻ 0.001) without affecting the lower plateau of SNA (from 12.5 Ϯ 2.4% to 9.5 Ϯ 2.5% in WKY, and from 28.8 Ϯ 2.8% to 30.4 Ϯ 5.7% in SHR, P ϭ 0.800) in the neural arc. While tempol did not affect the peripheral arc characteristics in WKY, it yielded a downward change in the regression line of AP vs. SNA in SHR. In conclusion, oxidative redox signaling plays an important role, not only in the pathological AP elevation, but also in the baroreflex-mediated physiological AP regulation. The effect of modulating oxidative redox signaling on the peripheral arc contributed to the determination of AP in SHR but not in WKY.carotid sinus baroreflex; open-loop analysis; sympathetic nerve activity; equilibrium diagram OXIDATIVE REDOX SIGNALING is considered to play an important role in the pathogenesis of hypertension via various effects on both the vasculature and the sympathetic nervous system. ANG II stimulates NADH/NADPH oxidase activity in cultured vascular smooth muscle cells and increases superoxide anion production (6, 29). In spontaneously hypertensive rats (SHR), the production of superoxide anion is elevated in aortic vessels, and the application of tempol (2,2,6,6-tetramethyl-4-piperidinol-N-oxyl), a membrane-permeable superoxide dismutase mimetic, acutely reduces the production of superoxide anion to a level similar to that observed in normotensive Wistar-Kyoto (WKY) rats (26). Perfusion with tempol attenuates the ANG II-induced vasoconstrictor response of the mesenteric vascular bed in SHR (25). The neural effect of oxidative redox signaling also involves NADH/NADPH oxidase-derived reactive oxygen species, which may play an important role in the sympathoexcitation induced by central ANG II administration (4). Systemic administration of tempol acutely reduces sympathetic ...

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Effects of tempol on baroreflex neural arc versus peripheral arc in normotensive and spontaneously hypertensive rats

Kawada

Sata

Shimizu

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Among them, the baroreflex system is an important and powerful regulator. 18,21,22) We developed a baroreflex failure model in rats with normal left ventricular function, and assessed the left atrial pressure (LAP) responses to volume overload. 23) We investigated the effect of baroreflex failure on LAP and systemic AP responses to volume loading in rats with normal left ventricular function in which baroreflex failure was mimicked by maintaining constant carotid sinus pressure (CSP).…”

Section: 14-17)mentioning

confidence: 99%

Heart Failure as a Disruption of Dynamic Circulatory Homeostasis Mediated by the Brain

Kishi

2016

Int. Heart J.

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SummaryCirculatory homeostasis is associated with interactions between multiple organs, and the disruption of dynamic circulatory homeostasis could be considered as heart failure. The brain is the central unit integrating neural and neurohormonal information from peripheral organs and controlling peripheral organs using the autonomic nervous system. Heart failure is worsened by abnormal sympathoexcitation associated with baroreflex failure and/or chemoreflex activation, and by vagal withdrawal, and autonomic modulation therapies have benefits for heart failure. Recently, we showed that baroreflex failure induces striking volume intolerance independent of left ventricular dysfunction. Many studies have indicated that an overactive renin-angiotensin system, excess oxidative stress and excess inflammation, and/or decreased nitric oxide in the brain cause sympathoexcitation in heart failure. We have demonstrated that angiotensin II type 1 receptor (AT 1 R)-induced oxidative stress in the rostral ventrolateral medulla (RVLM), which is known as a vasomotor center, causes prominent sympathoexcitation in heart failure model rats. Interestingly, systemic infusion of angiotensin II directly affects brain AT 1 R with sympathoexcitation and left ventricular diastolic dysfunction. Moreover, we have demonstrated that targeted deletion of AT 1 R in astrocytes strikingly improved survival with prevention of left ventricular remodeling and sympathoinhibition in myocardial infarction-induced heart failure. From these results, we believe it is possible that AT 1 R in astrocytes, not in neurons, have a key role in the pathophysiology of heart failure. We would like to propose a novel concept that the brain works as a central processing unit integrating neural and hormonal input, and that the disruption of dynamic circulatory homeostasis mediated by the brain causes heart failure. (Int Heart J 2016; 57: 145-149)

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“…22 We cut the vagal and aortic depressor nerves bilaterally. Two short sections of polyethylene tubing (PE-50) were placed into both carotid sinuses and connected to a fluid-filled transducer (DX-200, Viggo-Spectramed) and to a servo-controlled pump system based on an electromagnetic shaker and linear power amplifier (ARB-126, AR Brown).…”

Section: Animals and Surgical Proceduresmentioning

confidence: 99%

“…Anesthetic agents used in the present study could also affect the dynamic properties of arterial baroreflex control of SAP. Although we used a linear approach for estimating the dynamic properties of arterial baroreflex, the nonlinear nature of the arterial baroreflex system such as threshold and saturation phenomena 4,20,22 has been well known. Therefore our results should be interpreted carefully.…”

Section: Study Limitationsmentioning

confidence: 99%

Novel Therapeutic Strategy Against Central Baroreflex Failure

et al. 1999

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Background-Central baroreflex failure in Shy-Drager syndrome and traumatic spinal cord injuries results in severe orthostatic hypotension and often confines the patient to the bed. We proposed a novel therapeutic strategy against central baroreflex failure: implementation of an artificial feedback control system able automatically to regulate sympathetic vasomotor tone, that is, a bionic baroreflex system (BBS). With the use of a rat model of central baroreflex failure, we developed the BBS and tested its efficacy. Methods and Results-Our prototype BBS for the rat consisted of a pressure sensor placed into the aortic arch, stimulation electrodes implanted into the greater splanchnic nerve, and a computer-driven neural stimulator. By a white noise approach for system identification, we first estimated the dynamic properties underlying the normal baroreflex control of systemic arterial pressure (SAP) and then determined how the BBS computer should operate in real time as the artificial vasomotor center to mimic the dynamic properties of the native baroreflex. The open-loop transfer function of the artificial vasomotor center was identified as a high-pass filter with a corner frequency of 0.1 Hz. We evaluated the performance of the BBS in response to rapid-progressive hypotension secondary to sudden sympathetic withdrawal evoked by the local imposition of a pressure step on carotid sinus baroreceptors in 16 anesthetized rats. Without the BBS, SAP rapidly fell by 49Ϯ8 mm Hg in 10 seconds. With the BBS placed on-line with real-time execution, the SAP fall was suppressed by 22Ϯ6 mm Hg at the nadir and by 16Ϯ5 mm Hg at the plateau. These effects were statistically indistinguishable from those of the native baroreflex system. Conclusions-These results suggest the feasibility of a BBS approach for central baroreflex failure. (Circulation.1999;100:299-304.)

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New simple methods for isolating baroreceptor regions of carotid sinus and aortic depressor nerves in rats

Cited by 73 publications

References 15 publications

Effects of tempol on baroreflex neural arc versus peripheral arc in normotensive and spontaneously hypertensive rats

Effects of tempol on baroreflex neural arc versus peripheral arc in normotensive and spontaneously hypertensive rats

Heart Failure as a Disruption of Dynamic Circulatory Homeostasis Mediated by the Brain

Novel Therapeutic Strategy Against Central Baroreflex Failure

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