Acute resetting of baroreceptor reflex in rabbits: a central component

1986 ◽  
Vol 250 (5) ◽  
pp. H866-H870 ◽  
Author(s):  
D. L. Kunze
Keyword(s):  
Arterial Pressure ◽  
Test Stimulus ◽  
Nerve Stimulation ◽  
Sympathetic Activity ◽  
Constant Stimulus ◽  
Baroreceptor Reflex ◽  
Pressure Response ◽  
Stimulus Period ◽  
Aortic Nerve ◽  
Stimulation Of

Electrical stimulation of the aortic nerve of the anesthetized rabbit was used to determine whether there is a central nervous system component to acute resetting of the baroreceptor reflex. After stimulation of the aortic nerve for 5 min at 10 Hz, a ramp test stimulus to the nerve produced a reflex arterial pressure response that was attenuated as compared with that produced by the same ramp prior to the five-min stimulation period. Renal sympathetic nerve activity was recorded simultaneously to determine whether a reduction in the magnitude of the reflex inhibition of sympathetic activity produced by the depressor nerve stimulation could account for the attenuated arterial pressure response. Renal activity during the test ramp was reduced to the same value both before and after the constant stimulus period and thus did not correlate with the attenuated pressure response. There was, however, prolonged inhibition of tonic sympathetic activity after the 5-min stimulus period such that during the test stimulus there was less sympathetic activity to inhibit. The results were similar when sympathetic activity was recorded from branches of the sciatic nerve and from thoracic postganglionic nerves. In these nerves the period of prolonged inhibition after aortic nerve stimulation was up to 5 min. The attenuated pressure response to baroreceptor nerve stimulation after a constant stimulus appears to reflect the reduced change in sympathetic activity rather than the value to which the sympathetic activity falls.

Aortic nerve-activated cardioinhibitory neurons and interneurons

1975 ◽  
Vol 229 (3) ◽  
pp. 783-789 ◽  
Author(s):  
J Schwaber ◽  
N Schneiderman
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Baroreceptor Reflex ◽  
Motor Nucleus ◽  
Vagus Nerves ◽  
Antidromic Activation ◽  
Medial Nucleus ◽  
Aortic Nerve ◽  
Dorsal Motor Nucleus ◽  
Stimulation Of

Unit activity evoked by electrical stimulation of the aortic and vagus nerves was recorded in the dorsal motor nucleus and nucleus solitarius of unanesthetized rabbits. Cardioinhibitory cells which showed antidromic activation to stimulation of the vagus nerve and synaptic activation to stimulation of the aortic nerve were localized in lateral dorsal motor nucleus 0.5-0.8 mm anterior of the obex. Additionally, units were found that appeared to be interneurons in the medullary pathway subserving baroreceptor reflex effects on cardioinhibitory neurons. These cells were activated by aortic, and usually vagus, nerve stimulation, appeared to be polysynaptically activated, and were located in medial nucleus solitarius rostral to the obex. Neurons reflecting a cardiac rhythm but not activated by aortic nerve stimulation were also observed.

Effects of aortic nerve stimulation on discharges of sympathetic neurons innervating rat tail artery and vein

1998 ◽  
Vol 275 (4) ◽  
pp. R942-R949 ◽  
Author(s):  
Christopher D. Johnson ◽  
Michael P. Gilbey
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Activity ◽  
Volume Expansion ◽  
Sympathetic Neurons ◽  
Data Set ◽  
Tail Artery ◽  
Aortic Nerve ◽  
Blood Volume Expansion ◽  
Rat Tail ◽  
Stimulation Of

Activity was recorded from postganglionic sympathetic neurons (PSNs) innervating either the caudal ventral artery (CVA) or a lateral vein (LV) of the tail circulation of anesthetized rats. The study sought to determine whether sympathetic activity directed at the CVA and LV was influenced by cardiovascular mechanoreceptor afferents and whether this effect was differential. Cardiac rhythmicity was not a robust component of either CVA PSN activity or LV PSN activity. Stimulation of an aortic nerve with short trains was followed by a decreased probability of discharge in both CVA and LV PSNs that was followed by a series of peaks that showed a constant periodicity that was not significantly different from that revealed by autocorrelogram analysis over the same data set. The latter dominant periodicity is referred to in this and related previous publications as the T rhythm. Furthermore, blood volume expansion and long-train aortic nerve stimulation produced a significant decrease in the frequency of the T rhythm. It is concluded that the CVA and LV sympathetic activity can be influenced by inputs from cardiovascular mechanoreceptors and that this effect is mediated in part by a modulation of the T rhythm.

Posterior hypothalamic influences on cardiovascular effects of aortic nerve stimulation

1989 ◽  
Vol 257 (6) ◽  
pp. H1994-H2000 ◽  
Author(s):  
J. K. Smith ◽  
K. W. Barron
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Posterior Hypothalamus ◽  
Hypothalamic Stimulation ◽  
Bipolar Electrode ◽  
Aortic Depressor Nerve ◽  
Aortic Nerve ◽  
Posterior Hypothalamic Stimulation ◽  
Stimulation Of

The purpose of this study was to examine the influence of stimulation of the posterior hypothalamus on the baroreflex responses produced by stimulation of the aortic depressor nerve. Animals were initially anesthetized and implanted with a bipolar electrode in the posterior hypothalamus. Three to 5 days later, animals were anesthetized with urethan, and the left aortic depressor nerve was dissected and placed on a bipolar platinum-iridium electrode. The effects of electrical stimulation of the posterior hypothalamus (0, 160, and 280 microA) were examined in baroreflex-intact and acutely sinoaortic baroreceptor-denervated animals, and the responses to aortic nerve stimulation (2, 8, 16, and 32 Hz) were examined during each level of hypothalamic stimulation. The first set of experiments was performed in baroreceptor-intact animals; e.g., in animals with arterial baroreceptor inputs intact from both carotid sinus regions in addition to intact right aortic baroreceptor afferent pathways. In that group, stimulation of the posterior hypothalamus attenuated the bradycardia and depressor effects of aortic nerve stimulation. When influences from other baroreceptor inputs were removed with acute sinoaortic baroreceptor denervation, posterior hypothalamic stimulation interrupted the reflex bradycardia due to aortic nerve stimulation; however, the depressor response to aortic nerve stimulation was not attenuated. Similar to the arterial pressure response, hypothalamic stimulation did not attenuate the decreases in mesenteric and iliac vascular resistance produced by aortic nerve stimulation in the baroreflex-denervated group. We conclude that posterior hypothalamic stimulation attenuates baroreflex-mediated bradycardia but does not alter baroreflex control of arterial pressure and peripheral vascular resistance.

Modulation of carotid sinus baroreceptor reflex by sciatic nerve stimulation

1975 ◽  
Vol 228 (5) ◽  
pp. 1535-1541 ◽  
Author(s):  
M Kumada ◽  
K Nogami ◽  
K Sagawa
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Sciatic Nerve ◽  
Arterial Pressure ◽  
Nerve Stimulation ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Baroreceptor Reflex ◽  
Equilibrium Pressure ◽  
Sciatic Nerve Stimulation

In anethetized, immobilized, and vagotomized cats we analyzed the effect of sciatic nerve stimulation (SNS) on the relationships between intrasinus pressure (ISP) and arterial pressure (AP) and between ISP and heart rate (HR). At each of seven ISP levels between 60 and 240 mmHg, AP and HR before and 20 s after the onset of SNS were plotted against ISP to obtain the ISP-AP and ISP-HR relationships before and during SNA. SNA caused increases in AP, HR, and total peripheral resistance (TPR) and a decrease in cardiac output (CO). SNS raised the equilibrium pressure (the value of AP at which AP equaled ISP), but it significantly (P smaller than 0.005) decreased the slope (or gain) of the ISP-AP relationship at ISP's between 90 and 150 mmHg. SNS also significantly (P smaller than 0.05) diminished the gain of ISP-HR relationship at ISP's between 120 and 210 mmHg. Modulation of the gain of ISP-AP relationship was ascribable to that of CO but not of TPR. We conclude that in vagotomized cats 1) SNS attenuates the sensitivity of AP and HR responses in the carotid sinus baroreceptor reflex, and 2) the inhibition of the reflex AP response was caused by modulation of the reflex CO response.

Central actions of angiotensin II oppose baroreceptor-induced sympathoinhibition

1984 ◽  
Vol 246 (1) ◽  
pp. R13-R19 ◽  
Author(s):  
R. D. Stein ◽  
R. B. Stephenson ◽  
L. C. Weaver
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Carotid Sinus ◽  
Sympathetic Neurons ◽  
Baroreceptor Reflex ◽  
Sympathetic Outflow ◽  
Afferent Activity ◽  
Neural Responses ◽  
Central Actions

Angiotensin II causes increased arterial pressure which may be mediated, in part, by effects on central sympathetic neurons or by interference with central or peripheral components of the baroreceptor reflex. This investigation was undertaken to determine actions of angiotensin II on sympathetic splanchnic efferent and carotid sinus afferent activity in chloralose-anesthetized cats. Neural responses during increases in arterial pressure caused by intracarotid or intravenous administration of angiotensin II were compared with responses to equivalent increases in arterial pressure induced by intravenously injected dextran or phenylephrine. Intracarotid injections of angiotensin II caused variable splanchnic sympathetic responses consisting of increased, decreased, or unchanged activity. In contrast, intravenous infusions of dextran or phenylephrine consistently inhibited sympathetic activity. Carotid sinus afferent activity was increased similarly by intracarotid angiotensin II and intravenous dextran or phenylephrine. Sympathetic and baroreceptor afferent responses to intravenously injected angiotensin II were not significantly different from responses to dextran or phenylephrine. These data demonstrate that angiotensin II can act centrally to excite sympathetic outflow or to interfere with inhibitory influences of arterial baroreceptors.

Effects of Percutaneous Stimulation of Both Sympathetic and Parasympathetic Cardiac Autonomic Nerves on Cardiac Function in Dogs

2012 ◽  
Vol 7 (4) ◽  
pp. 282-289 ◽  
Author(s):  
Mariko Kobayashi ◽  
Seiichiro Sakurai ◽  
Tohru Takaseya ◽  
Akira Shiose ◽  
Hyun-Il Kim ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Cardiac Function ◽  
Nerve Stimulation ◽  
Venous Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Electrode Placement ◽  
Autonomic Nerves ◽  
Stroke Work ◽  
Stimulation Of

Objective Augmentation of left ventricular (LV) contractility and heart rate (HR) by sympathetic nerve stimulation and amelioration of heart failure by vagal nerve stimulation has been reported. However, the effects of concomitant electrical stimulation of both sympathetic and parasympathetic cardiac nerves in tissues such as those of the cardiac plexus remain unclear. This study sought to assess acute changes in cardiac function and hemodynamics in response to endovascular cardiac plexus stimulation (CPS). Methods Twelve dogs received endovascular CPS via a bipolar catheter within the right pulmonary artery. Stimulation frequency (20 Hz) and pulse width (4 milliseconds) were fixed; voltage varied (range, 15–60 V). Results Results fell into three categories: 1, no response (n = 4); 2, an increase in systemic arterial pressure that was dependent on electrode placement (n = 4); and 3, a very reproducible and stable increase in aortic pressure (n = 4). In the third group, mean systolic aortic pressures, maximum value of the first derivative of LV pressure, and LV stroke work increased with stimulation (P < 0.02 for all parameters) as did cardiac output, end-systolic elastance, and preload recruitable stroke work (P = 0.03). Systemic and pulmonary vascular resistance, central venous pressure, pulmonary arterial pressure, and HR remained unchanged (P > 0.05). Conclusions In contrast to conventional inotropic agents, endovascular CPS induced significant and selective increases in LV contractility without increasing HR. Efforts to optimize electrode placement and fixation will improve the reproducibility of endovascular CPS treatment.

Characterization of midline medulla role in the trigeminal depressor response

1989 ◽  
Vol 256 (5) ◽  
pp. R1111-R1120 ◽  
Author(s):  
M. E. Clement ◽  
R. B. McCall
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Baroreceptor Reflex ◽  
Nerve Activity ◽  
Depressor Response ◽  
Reflex Activation ◽  
Stimulation Of

The purpose of the present investigation was to determine the role of the midline medulla in mediating the trigeminal depressor response. Previously we found that lesions of the midline medulla abolished the decrease in blood pressure resulting from electrical stimulation of the spinal trigeminal complex. Electrical stimulation (5 Hz) of the spinal trigeminal tract elicited a decrease in arterial blood pressure that was associated with an inhibition of sympathetic nerve activity recorded from the inferior cardiac nerve of anesthetized cats. The effect of single shocks applied to the trigeminal complex on sympathetic activity was determined using computer-averaging techniques. Single shock stimulation consistently elicited an excitation of sympathetic activity that was followed by an inhibition of sympathetic nerve discharge. The gamma-aminobutyric acid antagonist picrotoxin blocked the depressor response elicited by electrical stimulation of the midline medulla but not by stimulation of the spinal trigeminal complex. Extracellular recordings of the discharges of midline medullary neurons were made to determine the effects of trigeminal stimulation on sympathoinhibitory, sympathoexcitatory, and serotonin neurons. Sympathoinhibitory and sympathoexcitatory neurons were identified by the relationship between unitary discharges and sympathetic nerve activity and by their response to baroreceptor reflex activation. Serotonin (5-HT) neurons were identified using criteria previously developed in our laboratory. These included 1) a slow regular discharge rate, 2) sensitivity to the inhibitory action of the 5-HT1A agonist 8-OH 8-hydroxy-2-(di-n-propylamino)tetralin, 3) failure to respond to baroreceptor reflex activation, and 4) the discharges of the 5-HT neurons were not related to sympathetic activity. Stimulation of the spinal trigeminal complex typically inhibited the discharges of sympathoinhibitory neurons. In contrast, stimulation of the trigeminal complex consistently excited both sympathoexcitatory and 5-HT neurons. These results are discussed in relationship to the role of the midline medulla in mediating the trigeminal depressor response.

Diving responses in ducks after acute barodenervation

1983 ◽  
Vol 245 (2) ◽  
pp. R222-R229
Author(s):  
D. R. Jones ◽  
W. K. Milsom ◽  
F. M. Smith ◽  
N. H. West ◽  
O. S. Bamford
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Baroreceptor Reflex ◽  
Diving Response ◽  
Cardiac Control ◽  
Large Decline ◽  
Stimulation Of

The contribution of systemic arterial baroreceptors to the cardiovascular adjustments to diving has been investigated in unanesthetized ducks after acute baroreceptor denervation. Both intact and denervated ducks exhibited bradycardia on diving, although denervated ducks showed a lesser and more variable fall in heart rate. Hindlimb vascular resistance rose significantly in both intact and denervated ducks. Continuous stimulation of one depressor nerve, through miniature electrodes implanted on the cut central end, resulted in a diving bradycardia intermediate between that recorded in intact and denervated animals. Intermittent stimulation of the depressor nerve, for 20-s periods, at intensities high enough to cause a large fall in mean arterial pressure (MAP) predive caused a smaller reduction in MAP as a dive was prolonged, due to a large decline in the ability of the baroreceptor reflex to affect peripheral resistance. There was no change in the effect of stimulation on cardiac control before or during diving. The present experiments indicate that a barostatic reflex, which exerts its effects primarily through cardiac control and not control of total peripheral resistance, is active through the dive but that the majority of the diving response in ducks is independent of baroreceptor integrity.

Effects of Increased Reflex Sympathetic Activity on Contractile Force of the Heart

1957 ◽  
Vol 191 (3) ◽  
pp. 461-468 ◽  
Author(s):  
Marion deV. Cotten ◽  
Neil C. Moran
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Right Ventricular ◽  
Nerve Stimulation ◽  
Sympathetic Activity ◽  
Sympathetic Nerves ◽  
Contractile Force ◽  
Carotid Occlusion ◽  
Cardiac Contractile

Reflexly induced changes in cardiac contractile force and arterial pressure in vagotomized dogs were compared with those produced by direct postganglionic cardiac sympathetic nerve stimulation, by i.v. injections of l-norepinephrine and by elevation of the intracranial pressure. Bilateral carotid occlusion and central vagal and central sciatic nerve stimulation produced a marked rise in arterial pressure but only a moderate increase in right ventricular contractile force. In contrast, direct stimulation of the cardiac sympathetic nerves and selected doses of l-norepinephrine caused a marked increase in right ventricular contractile force with only moderate elevation of blood pressure. Further, reflex stimulation resulted in a moderate dilation of the left ventricle in contrast to a reduction in size produced by l-norepinephrine. Elevation of the intracranial pressure provoked marked increases in both blood pressure and right ventricular contractile force. Experiments with vagotomized cats gave comparable results. The moderate positive inotropic effect of carotid occlusion in dogs was mediated both through the cardiac sympathetic nerves and the adrenal glands since removal of either structure alone reduced the response while combined adrenalectomy and cardiac sympathectomy abolished the effect. These results indicate that the predominant effect of reflexly augmented sympathetic activity through the carotid sinus, vagus and sciatic nerves is on vasomotor tone with only moderate influence on cardiac contractile force.

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