scholarly journals Systematic understanding of acute effects of intravenous guanfacine on rat carotid sinus baroreflex-mediated sympathetic arterial pressure regulation

Life Sciences ◽  
2016 ◽  
Vol 149 ◽  
pp. 72-78 ◽  
Author(s):  
Toru Kawada ◽  
Shuji Shimizu ◽  
Michael J. Turner ◽  
Masafumi Fukumitsu ◽  
Hiromi Yamamoto ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Pressure Regulation ◽  
Acute Effects ◽  
Carotid Sinus Baroreflex ◽  
Systematic Understanding ◽  
Arterial Pressure Regulation

Peripheral versus central effect of intravenous moxonidine on rat carotid sinus baroreflex-mediated sympathetic arterial pressure regulation

Life Sciences ◽  
2017 ◽  
Vol 190 ◽  
pp. 103-109 ◽  
Author(s):  
Toru Kawada ◽  
Shuji Shimizu ◽  
Hiromi Yamamoto ◽  
Tadayoshi Miyamoto ◽  
Toshiaki Shishido ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Central Effect ◽  
Pressure Regulation ◽  
Carotid Sinus Baroreflex ◽  
Arterial Pressure Regulation

Center of arterial pressure regulation during rotation of normal and abnormal dogs

1963 ◽  
Vol 204 (6) ◽  
pp. 979-982 ◽  
Author(s):  
Edward E. Smith ◽  
Arthur C. Guyton
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Regulatory Mechanisms ◽  
Pressure Regulation ◽  
Transverse Axis ◽  
Total Spinal Anesthesia ◽  
Axis Of Rotation ◽  
Arterial Pressure Regulation

Dogs were rotated about a horizontal transverse axis. By shifting the axis of rotation along the length of the animal's body it was possible to find a point at which arterial pressure remained almost constant in all positions of rotation. In most normal dogs such an axis lay in the neck a few centimeters cephalad to the sternum. Denervation of carotid sinus and aortic pressoreceptors caused a caudal shift of the axis; total spinal anesthesia did also, and to a much greater degree. This study demonstrates that pressure regulatory mechanisms operate to maintain a constant arterial pressure in the neck, probably for the minimizing of postural alterations of cerebral blood flow

Neural arc of baroreflex optimizes dynamic pressure regulation in achieving both stability and quickness

1996 ◽  
Vol 271 (3) ◽  
pp. H882-H890 ◽  
Author(s):  
Y. Ikeda ◽  
T. Kawada ◽  
M. Sugimachi ◽  
O. Kawaguchi ◽  
T. Shishido ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Mechanical Response ◽  
Carotid Sinus ◽  
Dynamic Pressure ◽  
Open Loop ◽  
Pressure Regulation ◽  
Frequency Range ◽  
Sinus Pressure ◽  
Arterial Pressure Regulation

The baroreflex loop consists of a fast neural arc and a slow mechanical arc. We hypothesized that the neural baroreflex arc compensates the slow mechanical response and thus improves the quality of blood pressure regulation. We estimated the open-loop transfer characteristics of the neural baroreflex arc (HP), i.e., from carotid sinus pressure to sympathetic nerve activity (SNA), and that of the effective peripheral baroreflex arc (Hp), i.e., from SNA to arterial pressure, in anesthetized rabbits. The gain of Hn was constant below 0.12 +/- 0.057 Hz and increased with a slope of 6.1 +/- 0.06 dB/octave above its frequency up to 1 Hz. In contrast, the gain of Hp was constant below 0.071 +/- 0.03 Hz and decreased with a slope of -11.0 +/- 1.48 dB/octave above the frequency. These data indicate that Hn accelerates slow peripheral responses in the frequency range of 0.1-1 Hz. Although too much acceleration in the high-frequency range could result in instability of the system, numerical analysis of the closed-loop baroreflex response indicated that the neural arc optimized arterial pressure regulation in achieving both stability and quickness.

Inhibition of NO synthesis minimally affects the dynamic baroreflex regulation of sympathetic nerve activity

1997 ◽  
Vol 272 (5) ◽  
pp. H2446-H2452 ◽  
Author(s):  
H. Miyano ◽  
T. Kawada ◽  
T. Shishido ◽  
T. Sato ◽  
M. Sugimachi ◽  
...  
Keyword(s):  
Transfer Function ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Function Analysis ◽  
Corner Frequency ◽  
Nerve Activity ◽  
Carotid Sinus Baroreflex ◽  
Transfer Function Analysis

The purpose of this investigation was to examine the role of nitric oxide (NO) in the dynamic baroreflex regulation of cardiac sympathetic nerve activity. In anesthetized rabbits, we imposed random pressure perturbations on the isolated carotid sinuses before and after the intravenous administration of NG-monomethyl-L-arginine. We characterized the dynamic properties relating carotid sinus pressure input to sympathetic nerve activity by means of a transfer function analysis. NG-monomethyl-L-arginine decreased the corner frequency of the transfer function (0.100 +/- 0.054 vs. 0.074 +/- 0.035 Hz; P < 0.05), whereas other parameters such as the steady-state gain and transmission lag time remained unchanged. Although cursory examination of these findings would suggest a possible contribution of NO in the dynamic baroreflex regulation of sympathetic nerve activity, quantitative assessment of the transfer function reveals only a minimal effect on the baroreflex regulation of arterial pressure, particularly under closed-loop conditions. We conclude that NO noticeably affects the dynamic baroreflex regulation of sympathetic nerve activity. However, it may not significantly affect arterial pressure regulation through central modulation of the carotid sinus baroreflex.

The arterial depressor response to chronic low-dose angiotensin II infusion in female rats is estrogen dependent

2012 ◽  
Vol 302 (1) ◽  
pp. R159-R165 ◽  
Author(s):  
Amanda K. Sampson ◽  
Lucinda M. Hilliard ◽  
Karen M. Moritz ◽  
Merlin C. Thomas ◽  
Chris Tikellis ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Low Dose ◽  
Renin Angiotensin System ◽  
Female Rats ◽  
Ang Ii ◽  
Pressure Regulation ◽  
Estrogen Replacement ◽  
Sprague Dawley ◽  
Arterial Pressure Regulation

The complex role of the renin-angiotensin-system (RAS) in arterial pressure regulation has been well documented. Recently, we demonstrated that chronic low-dose angiotensin II (ANG II) infusion decreases arterial pressure in female rats via an AT2R-mediated mechanism. Estrogen can differentially regulate components of the RAS and is known to influence arterial pressure regulation. We hypothesized that AT2R-mediated depressor effects evident in females were estrogen dependent and thus would be abolished by ovariectomy and restored by estrogen replacement. Female Sprague-Dawley rats underwent ovariectomy or sham surgery and were treated with 17β-estradiol or placebo. Mean arterial pressure (MAP) was measured via telemetry in response to a 2-wk infusion of ANG II (50 ng·kg−1·min−1 sc) or saline. MAP significantly decreased in females treated with ANG II (−10 ± 2 mmHg), a response that was abolished by ovariectomy (+4 ± 2 mmHg) and restored with estrogen replacement (−6 ± 2 mmHg). Cardiac and renal gene expression of components of the RAS was differentially regulated by estrogen, such that overall, estrogen shifted the balance of the RAS toward the vasodilatory axis. In conclusion, estrogen-dependent mechanisms offset the vasopressor actions of ANG II by enhancing RAS vasodilator pathways in females. This highlights the potential for these vasodilator pathways as therapeutic targets, particularly in women.

Lack of time-dependent augmentation of carotid sinus baroreflex system after vagotomy

1982 ◽  
Vol 242 (4) ◽  
pp. H580-H584
Author(s):  
H. Hosomi ◽  
K. Yokoyama
Keyword(s):  
Control System ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Pressure Control ◽  
Open Loop ◽  
Carotid Sinus Baroreflex ◽  
Stepwise Reduction ◽  
Intact Condition ◽  
Pressure Control System ◽  
Arterial Pressure Control System

The purpose of this experiment was to study whether the carotid sinus baroreflex system (CS system) increases its gain with time after vagotomy in compensation for the loss of the vagally mediated arterial pressure control system (V system). In 7 dogs anesthetized with pentobarbital sodium we determined the responsiveness of the V system by repeatedly measuring the overall open-loop gain (G) of the negative feedback control system. G was assessed as (delta API/delta APS) -- 1, where delta API and delta APS are, respectively, the immediate and steady-state falls in arterial pressure at the aortic arch following a stepwise reduction in blood volume. delta API, delta APS, and G in intact condition were -12.0 +/- 1.8 mmHg, -1.1 +/- 0.2 mmHg, and 10.1 +/- 0.7 (SD), respectively. delta API, delta APS, and G after vagotomy, i.e., G of the CS system (GCS), were -15.6 +/- 3.6 mmHg, -6.4 +/- 1.9 mmHg, and 1.6 +/- 0.4 GCS did not change with time over 4 h after vagotomy. We conclude that the CS system cannot augment its ability to restore arterial pressure in compensation for the lost function of the V system within 4 h after vagotomy in the anesthetized dog.

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