Sympathetic responses to stimulation of area postrema in decerebrate and anesthetized rats

1995 ◽  
Vol 268 (3) ◽  
pp. H1086-H1095 ◽  
Author(s):  
A. A. Hegarty ◽  
L. F. Hayward ◽  
R. B. Felder
Keyword(s):  
Electrical Stimulation ◽  
Excitatory Amino Acid ◽  
Area Postrema ◽  
Neuronal Cell ◽  
Renal Sympathetic Nerve Activity ◽  
Pentobarbital Sodium ◽  
Anesthetized Rats ◽  
Neuronal Cell Bodies ◽  
Decerebrate Rat ◽  
Stimulation Of

The effects of electrical and chemical stimulation of the area postrema (AP) on mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) were examined in urethan- and pentobarbital sodium-anesthetized rats and in unanesthetized decerebrate rats. The AP was electrically stimulated over a range of frequencies (10–100 Hz) and intensities (10–80 microA) with a pulse duration of 0.2 or 1.0 ms. The excitatory amino acid L-glutamate (100 or 200 mM) was microinjected into the AP to preferentially stimulate neuronal cell bodies. In urethan-anesthetized rats, electrical stimulation of the AP decreased MAP and RSNA. In pentobarbital sodium-anesthetized rats, MAP and RSNA were markedly increased by AP stimulation. In unanesthetized decerebrate rats, increases in MAP and RSNA were also observed during electrical AP stimulation. Microinjection of L-glutamate had no effect on MAP and RSNA in anesthetized or in unanesthetized rats. These results indicate that electrical AP stimulation increases sympathetic output in the unanesthetized decerebrate rat and that anesthesia modifies this sympathetic response. The findings also suggest that peripheral responses to L-glutamate and electrical stimulation of the AP are mediated over different central pathways.

Excitatory amino acid receptors in commissural nucleus of the NTS mediate carotid chemoreceptor responses

1993 ◽  
Vol 264 (1) ◽  
pp. R41-R50 ◽  
Author(s):  
A. Vardhan ◽  
A. Kachroo ◽  
H. N. Sapru
Keyword(s):  
Amino Acid ◽  
Carotid Body ◽  
Excitatory Amino Acid ◽  
Minute Ventilation ◽  
Neuronal Cell ◽  
Excitatory Amino Acid Receptors ◽  
Amino Acid Receptors ◽  
Neuronal Cell Bodies ◽  
Carotid Body Chemoreceptors ◽  
Stimulation Of

Stimulation of carotid body chemoreceptors by saline saturated with 100% CO2 elicited an increase in mean arterial pressure, respiratory rate, tidal volume, and minute ventilation (VE). Microinjections of L-glutamate into a midline area 0.5-0.75 mm caudal and 0.3-0.5 mm deep with respect to the calamus scriptorius increased VE. Histological examination showed that the site was located in the commissural nucleus of the nucleus tractus solitarii (NTS). The presence of excitatory amino acid receptors [N-methyl-D-aspartic acid (NMDA); kainate, quisqualate/alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and trans 1-amino-cyclopentane-trans-1,3-dicarboxylic acid (ACPD)] in this area was demonstrated by microinjections of appropriate agonists. Simultaneous blockade of NMDA and non-NMDA receptors by combined injections of DL-2-aminophosphonoheptanoate (AP-7; 1 nmol) and 6,7-dinitro-quinoxaline-2,3-dione (DNQX; 1 nmol) abolished the responses to stimulation of carotid body on either side. Combined injections of AP-7 and DNQX did not produce a nonspecific depression of neurons because the responses to another agonist, carbachol, remained unaltered. Inhibition of the neurons in the aforementioned area with microinjections of muscimol (which hyperpolarizes neuronal cell bodies but not fibers of passage) also abolished the responses to subsequent carotid body stimulation on either side.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of vasopressin in sympathetic response to paraventricular nucleus stimulation in anesthetized rats

1994 ◽  
Vol 266 (1) ◽  
pp. R228-R236 ◽  
Author(s):  
S. C. Malpas ◽  
J. H. Coote
Keyword(s):  
Paraventricular Nucleus ◽  
Neuronal Cell ◽  
Detection Algorithm ◽  
Homocysteic Acid ◽  
Renal Sympathetic Nerve Activity ◽  
Anesthetized Rats ◽  
Neuronal Cell Bodies ◽  
Peak Detection Algorithm ◽  
Glass Micropipette

Vasopressin may play an extrahypothalamic role in the central control of the cardiovascular system, specifically acting as a spinal neurotransmitter in the pathway where the paraventricular nucleus (PVN) alters sympathetic outflow. In this study, the effect of stimulating neuronal cell bodies in the PVN on renal sympathetic nerve activity (RSNA) and the possible involvement of vasopressin in the pathway was investigated in anesthetized rats. The PVN was stimulated by microinjection with 0.2 M D,L-homocysteic acid via a glass micropipette, and the hemodynamic and sympathetic responses were recorded. A computerized sympathetic peak-detection algorithm was applied to recordings of sympathetic discharges to retrieve information about the characteristics of RSNA during PVN stimulation. The algorithm scanned the series of RSNA voltages for significant increases followed by significant decreases in a small cluster of voltage values. Once each synchronized RSNA peak had been detected, its corresponding amplitude and peak-to-peak interval were calculated. PVN stimulation consistently increased the amplitude of RSNA (mean 30 +/- 5.6% over control), arterial pressure, and the peak-to-peak interval of discharges. A V1 vasopressin antagonist intrathecally administered as a 500-pmol dose was subsequently able to completely block the hemodynamic response (blood pressure increase of 14 +/- 5%) and a 35 +/- 6% increase in RSNA in response to PVN stimulation and intrathecal vasopressin. Thus spinal vasopressin is likely to be a neurotransmitter involved in the cardiovascular regulation involving the PVN.

Role of baroreceptor afferents on area postrema-induced inhibition of sympathetic activity

1991 ◽  
Vol 260 (4) ◽  
pp. H1353-H1358
Author(s):  
M. Hay ◽  
E. M. Hasser ◽  
K. P. Undesser ◽  
V. S. Bishop
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Activity ◽  
Area Postrema ◽  
Afferent Input ◽  
Dependent Manner ◽  
Chemical Application ◽  
Renal Sympathetic Nerve Activity ◽  
Before And After ◽  
Stimulation Of

Activation of the area postrema by either electrical stimulation or chemical application of L-glutamate has been shown to result in an enhancement of cardiovascular baroreflexes similar to that seen with systemic infusions of arginine vasopressin (AVP). In addition, it has been found that the effects of AVP on baroreflex inhibition of renal sympathetic nerve activity (RSNA) are similar to those observed with phenylephrine following lesions of the area postrema or after partial denervation of baroreceptor afferents. The present study was undertaken to determine the role of baroreceptor afferent input on area postrema stimulation-induced decreases in sympathetic activity. In anesthetized rabbits, the responses of arterial pressure, heart rate, and RSNA to area postrema electrical stimulation were obtained before and after progressive sinoaortic denervation and vagotomy. Stimulation of the area postrema in carotid sinus-denervated animals consistently decreased RSNA in a frequency-dependent manner. However, following bilateral removal of both the aortic nerves and the vagi, electrical stimulation of the area postrema had no effect on RSNA. These results suggest that the ability of area postrema stimulation to inhibit RSNA is dependent on the presence of baroreceptor afferent input.

Cardiovascular responses to chemical and electrical stimulation of amygdala in rats

1987 ◽  
Vol 253 (5) ◽  
pp. R712-R718 ◽  
Author(s):  
A. J. Gelsema ◽  
D. J. McKitrick ◽  
F. R. Calaresu
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Neuronal Cell ◽  
Cardiovascular Responses ◽  
Chemical Stimulation ◽  
Anatomic Site ◽  
Neuronal Cell Bodies ◽  
Cardiovascular Variables ◽  
Amygdaloid Nuclei ◽  
Stimulation Of

Electrical stimulation of the amygdala has been shown to produce changes in cardiovascular variables. To locate neuronal cell bodies responsible for these changes, responses of arterial pressure (AP) and heart rate (HR) to DL-homocysteate (DLH, 0.15 M, 50-100 nl) microinjected into sites in three amygdaloid nuclei were compared with responses to electrical (90-150 microA) stimulation of the same sites in 35 artificially ventilated, paralyzed, urethan-anesthetized rats. Electrical stimulation resulted in depressor responses in most sites (89%). Changes in AP were accompanied by variable changes in HR. Chemical stimulation produced significantly fewer (25%) depressor responses. Similar results were obtained with injections of 1.0 M DLH. To eliminate the influence of the anesthetic on these responses, AP was recorded in nine conscious rats while stimulating the amygdala. Changes in behavior and AP in these animals could be obtained only by electrical stimulation. These results may be interpreted to indicate either that cell bodies responsible for changes in cardiovascular variables during electrical stimulation are not located in the amygdala or that chemical and electrical stimulation affect different neuronal elements in circuits located in the same anatomic site.

Role of alpha-adrenergic mechanisms on responses to area postrema stimulation and circulating vasopressin

1993 ◽  
Vol 265 (2) ◽  
pp. H530-H536 ◽  
Author(s):  
E. M. Hasser ◽  
V. S. Bishop
Keyword(s):  
Electrical Stimulation ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Adrenergic Antagonist ◽  
Renal Sympathetic ◽  
Catecholaminergic Mechanisms ◽  
Stimulation Of

This study evaluated the role of catecholamines in the nucleus tractus solitarius (NTS) on the inhibition of renal sympathetic nerve activity (RSNA) due to direct electrical stimulation of the area postrema. In addition, the effects of catecholaminergic mechanisms in the NTS on the ability of circulating arginine vasopressin (AVP) to modulate arterial baroreflex control of RSNA were evaluated. Electrical stimulation of the area postrema (15 microA, 0.3 ms, 5-80 Hz) produced progressive decreases in RSNA. Responses to area postrema activation were not altered by microinjection of the alpha 1-adrenergic antagonist, prazosin, or vehicle bilaterally into the NTS. Microinjection of the alpha 2-antagonist, yohimbine (4 injections of 20-40 nl, 1 ng/nl), unilaterally into the NTS significantly attenuated the RSNA response to area postrema stimulation. Bilateral injection of yohimbine into the NTS abolished the response to area postrema activation (P < 0.05). Baroreflex inhibition of RSNA was significantly greater during infusion of AVP than during infusion of phenylephrine (slopes = -5.18 +/- 0.39 and -2.64 +/- 0.27 for AVP and phenylephrine, respectively). Microinjection of yohimbine bilaterally into the NTS did not alter the slope of baroreflex control of RSNA for phenylephrine but normalized the slope for AVP (-2.85 +/- 0.54) to that of phenylephrine. Data are consistent with the hypothesis that AVP effects on baroreflex inhibition of RSNA and area postrema-mediated inhibition of RSNA require alpha 2-adrenergic signaling within the NTS.

Estrogen enhancement of baroreflex sensitivity is centrally mediated

1999 ◽  
Vol 276 (4) ◽  
pp. R1030-R1037 ◽  
Author(s):  
Mohamed K. Mohamed ◽  
Mahmoud M. El-Mas ◽  
Abdel A. Abdel-Rahman
Keyword(s):  
Electrical Stimulation ◽  
Baroreflex Sensitivity ◽  
Hemodynamic Responses ◽  
Pentobarbital Sodium ◽  
Conscious Rats ◽  
Reflex Bradycardia ◽  
Aortic Nerve ◽  
Anesthetized Rats ◽  
Ovx Rats ◽  
Stimulation Of

We have recently shown that estrogen enhances baroreceptor control of reflex bradycardia in conscious rats. The present study replicated this finding in pentobarbital sodium-anesthetized rats, and the study was extended to investigate whether this effect of estrogen is centrally or peripherally mediated. Hemodynamic responses to electrical stimulation of the central end of the aortic depressor or the vagal efferent nerve were evaluated in pentobarbital sodium-anesthetized sham-operated (SO), ovariectomized (OVX), and OVX estradiol-treated Sprague-Dawley rats. Phenylephrine (1–16 μg/kg iv) elicited dose-dependent pressor and bradycardic responses. Regression analysis of the baroreflex curves, relating changes in mean arterial pressure and heart rate, revealed a significantly smaller baroreflex sensitivity in OVX compared with SO anesthetized rats (−0.54 ± 0.05 and −0.91 ± 0.12 beats ⋅ min−1 ⋅ mmHg−1, respectively; P < 0.05). Treatment of OVX rats with 17β-estradiol (E2, 50 μg ⋅ kg−1 ⋅ day−1for 2 days subcutaneously) significantly enhanced baroreflex sensitivity to a level similar to that of SO rats ( P < 0.05). The enhancing effect of E2 on the baroreflex-mediated bradycardia, observed in conscious and anesthetized rats, seems to be selective because the baroreflex-mediated tachycardic responses measured in a separate group of conscious rats were not altered by ovariectomy or E2 administration. Electrical stimulation of the aortic nerve elicited frequency-dependent depressor and bradycardic responses that were significantly smaller in OVX compared with SO values ( P < 0.05). Treatment of OVX rats with E2 restored the hemodynamic responses to aortic stimulation to near SO levels. On the other hand, hemodynamic responses to vagal stimulation were not affected by OVX or treatment with E2. These findings suggest that enhancement of reflex bradycardia by estrogen is centrally mediated and involves interaction with central projections of the aortic nerve.

scholarly journals Seminal Plug Expulsion Induced by Electrical Stimulation of the Intermesenteric Nerve in Anesthetized Rats

2007 ◽  
Vol 77 (4) ◽  
pp. 717-722 ◽  
Author(s):  
Jacques Bernabé ◽  
Pierre Clément ◽  
Pierre Denys ◽  
Laurent Alexandre ◽  
François Giuliano
Keyword(s):  
Electrical Stimulation ◽  
Anesthetized Rats ◽  
Stimulation Of

Excitatory amino acid receptors within NTS mediate arterial chemoreceptor reflexes in rats

1993 ◽  
Vol 265 (2) ◽  
pp. H770-H773 ◽  
Author(s):  
W. Zhang ◽  
S. W. Mifflin
Keyword(s):  
Electrical Stimulation ◽  
Amino Acid ◽  
Receptor Antagonist ◽  
Carotid Body ◽  
Excitatory Amino Acid ◽  
Pressor Responses ◽  
Carotid Body Chemoreceptors ◽  
Arterial Chemoreceptor ◽  
Stimulation Of ◽  
Arterial Baroreceptor

The nucleus tractus solitarius (NTS) is the primary site of termination of arterial baroreceptor and chemoreceptor afferent fibers. Excitatory amino acid (EAA) receptors within NTS have been shown to play an important role in the mediation of arterial baroreceptor reflexes; however, the importance of EAA receptors within NTS in the mediation of arterial chemoreceptor reflexes remains controversial. Therefore, in chloralose-urethan-anesthetized, mechanically ventilated, paralyzed rats, 4 nmol of the broad-spectrum EAA receptor antagonist kynurenic acid (Kyn) was injected into the NTS to observe the effects of EAA receptor blockade on the pressor responses evoked by either activation of ipsilateral carotid body chemoreceptors (by close arterial injection of CO2-saturated bicarbonate) or electrical stimulation of ipsilateral carotid sinus nerve (CSN). Under control conditions, activation of carotid body chemoreceptors and CSN stimulation evoked increases in arterial pressure of 27 +/- 2 (n = 24 sites) and 28 +/- 3% (n = 8), respectively. Kyn microinjection into NTS significantly reduced the pressor responses evoked by activation of carotid body chemoreceptors and electrical stimulation of the CSN for 20 and 25 min, respectively. Attenuation of pressor responses evoked by chemoreceptor activation were maximal at 20 min post-Kyn injection (13 +/- 2%), whereas CSN-evoked pressor responses were maximally attenuated at 15 min (6 +/- 4%). Microinjection into NTS of 4 nmol of xanthurenic acid, a structural analogue of Kyn with no EAA receptor antagonist properties, had no effect on chemoreceptor reflexes. We conclude that EAA receptors within NTS play an important role in the mediation of arterial chemoreceptor reflexes.

Neurons controlling cardiovascular responses to emotion are located in lateral hypothalamus-perifornical region

1990 ◽  
Vol 259 (5) ◽  
pp. R943-R954 ◽  
Author(s):  
O. A. Smith ◽  
J. L. DeVito ◽  
C. A. Astley
Keyword(s):  
Electrical Stimulation ◽  
Lateral Hypothalamus ◽  
Axonal Degeneration ◽  
Neuronal Cell ◽  
Cardiovascular Responses ◽  
Ibotenic Acid ◽  
Defense Reaction ◽  
Autonomic Responses ◽  
Neuronal Cell Bodies ◽  
Thoracic Cord

We did four experiments to determine whether the lateral hypothalamus-perifornical (LH/PF) region is the source of neuronal cell bodies responsible for producing the cardiovascular (CV) responses associated with emotion or the defense reaction. Of particular concern was whether the paraventricular nucleus (PVN) plays a role in the generation of these CV responses. Mapping the hypothalamus with electrical stimulation showed that the CV pattern of responses was never produced by stimulating the PVN and was invariably produced by stimulating the LH/PF region. Complete electrolytic destruction of the PVN and subsequent axonal degeneration did not change the CV pattern of responses elicited by LH/PF stimulation, whereas any encroachment of the lesion on the LH/PF region decreased the magnitude of the CV responses. Injection of the neuroexcitotoxin ibotenic acid (Ibo) into the PVN did not affect responses to LH/PF stimulation, whereas Ibo injection into the LH/PF region eliminated or severely attenuated the CV responses. Retrograde labeling of cells from the thoracic cord and the ventrolateral reticular formation revealed a scattered group of cells in the LH/PF region that may be the cells controlling the CV responses. These results point directly to the LH/PF region as the source of the cell bodies responsible for the autonomic responses associated with emotion or defense reactions.

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