Maintenance of carotid baroreflex function in advanced age in the rat

To evaluate the influence of age per se on the carotid sinus baroreceptors in the absence of hypertension and atherosclerosis, we employed the Fischer 344 rat model. In 14 adult (A, 6-9 mo) and 9 senescent (S, 24-26 mo) normotensive male Fischer 344 rats the left carotid sinus region was vascularly isolated with sinus nerve intact and perfused with oxygenated modified Kreb's solution. Simultaneous measurements of intrasinus pressure and femoral arterial pressure response were obtained during linear pressure increases (20-200 mmHg) in the vascularly isolated sinus. There was no age difference in base-line arterial pressure or heart rate. Both age groups demonstrated similar positive relations between basal femoral arterial pressure and the magnitude of the femoral pressure response to equivalent carotid sinus pressures. There were similar estimated sinus volumes at onset of systemic response (39 +/- 1, A; 39 +/- 1 microliter, S), time to initial systemic pressure response (9 +/- 1, A; 7 +/- 1 s, S), mean rates of femoral pressure decline (1.8 +/- 0.3, A; 2.1 +/- 0.3 mmHg/s, S), and return to base line (1.5 +/- 0.3, A; 1.4 +/- 0.3 mmHg/s, S) as well as magnitudes of systolic (25 +/- 3, A; 26 +/- 4 mmHg, S) and diastolic (21 +/- 2 A; 22 +/- 4 mmHg, S) pressure drops. Thus, in the Fischer 344 rat model of aging, which differs from the human in that it is not complicated by hypertension or atherosclerosis, carotid sinus baroreflex function appears to be well maintained in senescence.

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

Life Sciences ◽

10.1016/j.lfs.2016.02.051 ◽

2016 ◽

Vol 149 ◽

pp. 72-78 ◽

Cited By ~ 5

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

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Contrasting effects of moderate vagal stimulation on heart rate and carotid sinus baroreflex-mediated sympathetic arterial pressure regulation in rats

Life Sciences ◽

10.1016/j.lfs.2011.07.026 ◽

2011 ◽

Vol 89 (13-14) ◽

pp. 498-503 ◽

Cited By ~ 13

Author(s):

Toru Kawada ◽

Shuji Shimizu ◽

Meihua Li ◽

Atsunori Kamiya ◽

Kazunori Uemura ◽

...

Keyword(s):

Heart Rate ◽

Arterial Pressure ◽

Carotid Sinus ◽

Vagal Stimulation ◽

Pressure Regulation ◽

Carotid Sinus Baroreflex ◽

Arterial Pressure Regulation

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.272.5.h2446 ◽

1997 ◽

Vol 272 (5) ◽

pp. H2446-H2452 ◽

Cited By ~ 6

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.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1982.242.4.h580 ◽

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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Mucosal Immunization with Live Attenuated Francisella novicida U112ΔiglB Protects against Pulmonary F. tularensis SCHU S4 in the Fischer 344 Rat Model

PLoS ONE ◽

10.1371/journal.pone.0047639 ◽

2012 ◽

Vol 7 (10) ◽

pp. e47639 ◽

Cited By ~ 17

Author(s):

Aimee L. Signarovitz ◽

Heather J. Ray ◽

Jieh-Juen Yu ◽

M. N. Guentzel ◽

James P. Chambers ◽

...

Keyword(s):

Rat Model ◽

Mucosal Immunization ◽

Francisella Novicida ◽

Fischer 344 ◽

Fischer 344 Rat ◽

Schu S4

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Baroreflex responsiveness is maintained during isometric exercise in humans

Journal of Applied Physiology ◽

10.1152/jappl.1986.61.2.797 ◽

1986 ◽

Vol 61 (2) ◽

pp. 797-803 ◽

Cited By ~ 38

Author(s):

T. J. Ebert

Keyword(s):

Mean Arterial Pressure ◽

Arterial Pressure ◽

Carotid Sinus ◽

Maximum Voluntary Contraction ◽

Transmural Pressure ◽

Handgrip Exercise ◽

Isometric Handgrip ◽

Baroreflex Control ◽

Baroreflex Function ◽

Isometric Handgrip Exercise

The simultaneous rise in heart rate and arterial pressure during isometric handgrip exercise suggests that arterial baroreflex control may be altered. We applied incremental intensities of neck suction and pressure to nine healthy young men to alter carotid sinus transmural pressure. Carotid stimuli were delivered during 1) supine control, 2) “anticipation” of beginning exercise, and 3) handgrip (20% of maximum voluntary contraction). Anticipation was a quiet period, immediately preceding the beginning of handgrip, when no muscular work was being performed. Compared with control, the R-R interval prolongation and mean arterial pressure decline provoked by carotid stimuli were decreased during the anticipation period. These data suggest that influences from higher central neural locations may alter baroreflex function. Furthermore, we derived stimulus-response curves relating carotid sinus transmural pressure to changes in R-R interval and mean arterial pressure. These curves were shifted during handgrip; however, calculated regression slopes were not changed from control. The data indicate that isometric handgrip exercise has a specific influence on human carotid baroreflex control of arterial pressure and heart period: baroreflex function curves are shifted rightward during handgrip, whereas baroreflex sensitivity is unchanged. Furthermore, central neural influences may be partially involved in these alterations.

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Diabetes mellitus attenuates the pressure response against hypotensive stress by impairing the sympathetic regulation of the baroreflex afferent arc

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00515.2018 ◽

2019 ◽

Vol 316 (1) ◽

pp. H35-H44

Author(s):

Kazuhiro Kamada ◽

Keita Saku ◽

Takeshi Tohyama ◽

Toru Kawada ◽

Hiroshi Mannoji ◽

...

Keyword(s):

Diabetes Mellitus ◽

Arterial Pressure ◽

Control Theory ◽

Open Loop ◽

Pressure Response ◽

Response Threshold ◽

Loop Gain ◽

Baroreflex Function ◽

Sympathetic Regulation

Patients with diabetes mellitus (DM) often show arterial pressure (AP) lability associated with cardiovascular autonomic neuropathy. Because the arterial baroreflex tightly regulates AP via sympathetic nerve activity (SNA), we investigated the systematic baroreflex function, considering the control theory in DM by open-loop analysis. We used Zucker diabetic fatty (ZDF) rats as a type 2 DM model. Under general anesthesia, we isolated the carotid sinuses from the systemic circulation, changed intracarotid sinus pressure (CSP), and recorded SNA and AP responses. We compared CSP-AP (total loop), CSP-SNA (afferent arc), and SNA-AP (efferent arc) relationships between ZDF lean ( n = 8) and ZDF fatty rats ( n = 6). Although the total loop gain of baroreflex (ΔAP/ΔCSP) at the operating point did not differ between the two groups, the average gain in the lower CSP range was markedly reduced in ZDF fatty rats (0.03 ± 0.01 vs. 0.87 ± 0.10 mmHg/mmHg, P < 0.001). The afferent arc showed the same trend as the total loop, with a response threshold of 139.8 ± 1.0 mmHg in ZDF fatty rats. There were no significant differences in the gain of efferent arc between the two groups. Simulation experiments indicated a markedly higher AP fall and lower total loop gain of baroreflex in ZDF fatty rats than in ZDF lean rats against hypotensive stress because the efferent arc intersected with the afferent arc in the SNA unresponsive range. Thus, we concluded that impaired baroreflex sympathetic regulation in the lower AP range attenuates the pressure response against hypotensive stress and may partially contribute to AP lability in DM. NEW & NOTEWORTHY In this study, we investigated the open-loop baroreflex function, considering the control theory in type 2 diabetes mellitus model rats to address the systematic mechanism of arterial pressure (AP) lability in diabetes mellitus. The unresponsiveness of baroreflex sympathetic regulation in the lower AP range was observed in type 2 diabetic rats. It may attenuate the baroreflex pressure-stabilizing function and induce greater AP fall against hypotensive stress.

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Role of active changes in venous capacity by the carotid baroreflex: analysis with a mathematical model

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.267.6.h2531 ◽

1994 ◽

Vol 267 (6) ◽

pp. H2531-H2546 ◽

Cited By ~ 16

Author(s):

M. Ursino ◽

M. Antonucci ◽

E. Belardinelli

Keyword(s):

Mathematical Model ◽

Arterial Pressure ◽

Cardiovascular System ◽

Carotid Sinus ◽

Regulatory Mechanisms ◽

Unstressed Volume ◽

Carotid Sinus Baroreflex ◽

Left And Right ◽

Venous Capacity

To elucidate the role of venous capacity active changes in short-term cardiovascular homeostasis, a mathematical model of the carotid-sinus baroreflex system has been developed. In the model the cardiovascular system is represented as the series arrangement of six lumped compartments, which synthesize the fundamental hemodynamic properties of the systemic arterial, systemic venous, pulmonary arterial, and pulmonary venous circulations as well as of the left and right cardiac volumes. Cardiac outputs from the left and right ventricles are computed as a function of both downstream arterial pressure (afterload) and upstream atrial pressure (preload). Four distinct feedback regulatory mechanisms, working on systemic arterial resistance, heart rate, systemic venous unstressed volume, and systemic venous compliance, are assumed to operate on the cardiovascular system in response to carotid sinus pressure changes. All model parameters, both in the cardiovascular system and in feedback regulatory mechanisms, have been assigned on the basis of physiological data now available. The model is used here to simulate the pattern of the main hemodynamic quantities in the short time period (1-2 min) after acute carotid sinus activation in vagotomized subjects. Simulation results indicate that the model can reproduce experimental data quite well, with reference both to open-loop experiments and to an acute blood hemorrhage performed in closed-loop conditions. Moreover, computer simulations indicate that active changes in venous unstressed volume are of primary importance in regulating cardiac output and systemic arterial pressure during activation of the carotid sinus baroreflex.

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