Mechanisms of pressor response produced by stimulation of nucleus ambiguus

1990 ◽  
Vol 259 (5) ◽  
pp. R955-R962
Author(s):  
B. H. Machado ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Pressor Responses ◽  
Regional Vascular Resistance ◽  
Parasympathetic Control ◽  
Renal Vascular ◽  
Stimulation Of

We showed previously that activation of nucleus ambiguus (NA) induced bradycardia and increased arterial pressure. In this study, we compared responses produced by electrical and chemical (glutamate) stimulation of NA and adjacent rostral ventrolateral medulla (RVLM). Equivalent pressor responses were elicited from both areas. However: 1) The response from RVLM was elicited at a lower frequency. 2) Regional vascular resistance changes were different, i.e., electrical stimulation of NA increased vascular resistance in hindquarters much more than the renal and mesenteric beds. In contrast, electrical and chemical stimulation of RVLM produced a more prominent effect on the renal vascular bed. 3) Bradycardia was elicited from NA at lower current intensity. 4) Glutamate produced bradycardia only when injected into NA. Studies in rats with sinoaortic deafferentation showed that bradycardic response to activation of NA was only partly reflex in origin. We conclude that 1) NA and RVLM control sympathetic outflow to regional vascular beds differentially and 2) the NA region involves parasympathetic control of heart rate and sympathetic control of arterial pressure.

Vasoconstrictor and vasodilator sites within anteroventral third ventricle region

1987 ◽  
Vol 253 (6) ◽  
pp. R827-R831 ◽  
Author(s):  
M. L. Mangiapane ◽  
M. J. Brody
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Third Ventricle ◽  
Renal Vascular Resistance ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Tungsten Microelectrode ◽  
Renal Vascular ◽  
Stimulation Of

Previous studies have shown that electrical stimulation of the rat anteroventral third ventricle (AV3V) region produces a characteristic pattern of hemodynamic effects, i.e., renal and mesenteric vasoconstriction, and hindquarters vasodilation. In the present study, we localized the vasoconstrictor and vasodilator effects to specific subregions of the AV3V. In urethan-anesthetized rats prepared with arterial catheters and pulsed Doppler flow probes, we assessed the effects of electrical stimulation of four nuclei within AV3V on mean arterial pressure and renal, mesenteric, and hindquarters resistance. These nuclei were the organum vasculosum lamina terminalis (OVLT), ventral nucleus medianus (median preoptic nucleus), anterior (precommissural) nucleus medianus (median preoptic nucleus), and periventricular preoptic nuclei. Stimulation was carried out by use of a tungsten microelectrode. Stimulation of the OVLT consistently provoked stimulus-locked increases in arterial pressure coupled with increases in mesenteric and renal vascular resistance. Ganglionic blockade with chlorisondamine prevented these responses, demonstrating that they were mediated neurogenically. Stimulation of the three remaining nuclei produced decreases in arterial pressure, hindquarters vasodilation, and little change in mesenteric and renal vascular resistance. No changes in heart rate were observed with stimulation of any of the four nuclei. These results suggest that the vasoconstrictor and pressor functions of the AV3V region are localized in or near the OVLT region, whereas the remaining nuclei of the AV3V region mediate vasodilator and depressor responses.

Pressor response from rostral dorsomedial medulla is mediated by excitatory amino acid receptors in rostral VLM

1994 ◽  
Vol 267 (1) ◽  
pp. R309-R315 ◽  
Author(s):  
Y. Hirooka ◽  
J. W. Polson ◽  
R. A. Dampney
Keyword(s):  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Amino Acid Receptors ◽  
Control Value ◽  
Afferent Fibers ◽  
Pressor Responses ◽  
Before And After ◽  
Stimulation Of

Excitatory amino acid (EAA) receptors in the rostral part of the ventrolateral medulla (VLM) have been shown to mediate pressor responses elicited by stimulation of various peripheral afferent fibers as well as other central nuclei. This study tested the hypothesis that these receptors are a critical component in the central pathway mediating the powerful pressor response that is produced by stimulation of a group of neurons within a circumscribed region in the rostral dorsomedial medulla (RDM). In anesthetized rabbits, the pressor response elicited by unilateral microinjection of glutamate into this RDM region was measured before and after injection of kynurenic acid (Kyn), a broad-spectrum EAA receptor antagonist, into the physiologically identified pressor region of either the ipsilateral or contralateral rostral VLM. The pressor response to RDM stimulation was greatly reduced (to 24 +/- 4% of control) 5-10 min after injection of Kyn (but not the vehicle solution) into the ipsilateral rostral VLM; this response returned completely to its control value within 30-60 min after Kyn injection. By contrast, after Kyn injection into the contralateral rostral VLM, the pressor response to RDM stimulation was not affected (106 +/- 15% of control). The results indicate that the descending pressor pathway from the RDM to the spinal cord is mediated by EAA receptors in the rostral VLM pressor region. Furthermore, the pathway from the RDM to the rostral VLM is predominantly, if not exclusively, ipsilateral.

Mechanism of action of vasoconstrictor responses to atriopeptin II in conscious SHR

1985 ◽  
Vol 249 (6) ◽  
pp. R781-R786 ◽  
Author(s):  
R. W. Lappe ◽  
J. A. Todt ◽  
R. L. Wendt
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Sympathetic Nerves ◽  
Spontaneously Hypertensive ◽  
Regional Vascular Resistance ◽  
6 Hydroxydopamine ◽  
Renal Vascular ◽  
Renal Sympathetic

Previous studies have demonstrated that infusion of synthetic atriopeptin II (AP II) lowered arterial pressure, reduced regional blood flow, and increased total peripheral and regional vascular resistances in conscious spontaneously hypertensive rats (SHR). This study was designed to examine the mechanism(s) involved in regional vasoconstrictor responses to AP II. In these experiments, hemodynamic actions of AP II were examined in control, 6-hydroxydopamine-treated (chemically sympathectomized), and renal-denervated groups of instrumented conscious SHR. Infusion of AP II (1 microgram X kg-1 X min-1) caused similar reductions in mean arterial pressure in control (-22 +/- 2 mmHg), chemically sympathectomized (-23 +/- 2 mmHg), and renal-denervated (-23 +/- 3 mmHg) SHR. In control SHR, AP II infusion reduced renal (-20 +/- 3%), mesenteric (-26 +/- 2%), and hindquarters (-18 +/- 10%) blood flow and increased regional vascular resistance in all three beds. Chemical sympathectomy prevented the fall in renal blood flow (RBF) and significantly abolished the regional vasoconstrictor responses to AP II infusion. In unilateral renal-denervated groups of SHR, AP II reduced renal vascular resistance (RVR) -11 +/- 3% but failed to alter RBF (-3 +/- 1%) in denervated kidneys. In contrast, RVR increased (20 +/- 7%) and RBF was significantly reduced (-29 +/- 3%) in contralateral-innervated kidneys. This study demonstrated that chemical or surgical destruction of renal sympathetic nerves abolished AP II-induced increases in RVR. These data further indicate that in conscious SHR the regional vasoconstrictor responses to AP II infusion appear to be mediated by increases in sympathetic tone rather than through direct vascular actions of AP II.

Projections from the periaqueductal gray (PAG) to the periambigual area: Relation to cholinergic vago-cardiac neurons

1993 ◽  
Vol 51 ◽  
pp. 292-293
Author(s):  
Shuang-jin Xu ◽  
Tilat A. Rizvi ◽  
Maorong Jiang ◽  
Matthew Ennis ◽  
Michael T. Shipley
Keyword(s):  
Behavioral Responses ◽  
Periaqueductal Gray ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Tract Tracing ◽  
Autonomic Responses ◽  
Pressor Responses ◽  
Tracing Techniques ◽  
Species Specific ◽  
Stimulation Of

Activation of the midbrain periaqueductal gray (PAG) elicits species specific defense reactions and marked autonomic adjustments. In agreement with recent studies by Bandler and colleagues in the cat, we found that activation of rostrocaudally-oriented, longitudinally organized columns in PAG elicit differential cardiovascular and behavioral responses. Activation of dorsolateral/lateral PAG produces aggressive/flight behaviors accompanied by pressor responses while stimulation of ventrolateral PAG produces immobility and depressor responses. The pathways mediating these selective behavioral and autonomic responses are poorly understood.The projection from PAG to the sympathoexcitatory zone in the rostral ventrolateral medulla is a likely substrate for PAG-evoked pressor responses. However, circuits mediating PAG-evoked depressor responses are not known. The present studies have identified a robust, focal projection from PAG to the nucleus ambiguus (NA), a potent depressor area in the ventral medulla. In addition, we have used tract tracing techniques and immunocytochemistry to examine the organization of PAG projections in relation to cholinergic preganglionic parasympathetic NA neurons that innervate the heart.

Analysis of hemodynamic variability after sinoaortic denervation in the conscious rat

1986 ◽  
Vol 251 (6) ◽  
pp. R1163-R1169 ◽  
Author(s):  
A. J. Trapani ◽  
K. W. Barron ◽  
M. J. Brody
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Mesenteric Arteries ◽  
Conscious Rat ◽  
Mean Values ◽  
Regional Vascular Resistance ◽  
Renal Vascular ◽  
Relationship Of ◽  
The Relationship

The present study was undertaken to determine the regional hemodynamic basis for increased mean arterial pressure (MAP) variability produced by sinoaortic baroreceptor denervation (SAD) in the conscious rat. Sinoaortic-denervated and intact rats were instrumented chronically with a catheter placed in the femoral artery and pulsed-Doppler flow probes positioned on the renal and superior mesenteric arteries and the lower abdominal aorta to determine MAP, heart rate, and regional vascular resistance. Each cardiovascular variable was sampled once per minute during a 1-h recording period. Compared with control animals, baroreceptor-denervated animals exhibited greater variability of MAP and mesenteric, renal, and hindquarter resistances 7–9 days after SAD. The variability of heart rate was similar when animals from the two groups were compared. The pattern of significant correlation for the relationship of MAP to vascular resistance in the different beds was not consistent for individual SAD and intact animals. Finally, a wider distribution of mean values was observed for the individuals within the SAD group for MAP, heart rate, and hindquarter and renal vascular resistances. We conclude that SAD produces greater fluctuation of vascular resistance in several beds which contributes to the increased lability of MAP; however, there is no predictable pattern of vascular resistance lability which underlies the variability of arterial pressure.

Role of ventrolateral medulla in vasomotor response to cerebral ischemia

1980 ◽  
Vol 239 (3) ◽  
pp. H349-H358 ◽  
Author(s):  
R. A. Dampney ◽  
E. A. Moon
Keyword(s):  
Cerebral Ischemia ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Medullary Reticular Formation ◽  
Norepinephrine Infusion ◽  
Pressor Responses ◽  
Highly Sensitive ◽  
Dorsal Medulla ◽  
Stimulation Of

The ventrolateral medulla has been postulated to contain chemosensitive neurons. This study investigated the role of this region in the generation of the pressor response to cerebral ischemia (CIR) in anesthetized paralyzed artificially ventilated rabbits. A circumscribed and highly sensitive pressor area in the ventrolateral medullary reticular formation 2-4 mm rostral to the obex, separate from the well-known dorsal pressor area, was mapped by use of a stimulating electrode. Electrolytic destruction of this area resulted in a profound reduction in resting mean arterial pressure (MAP). After restoration of baseline MAP with norepinephrine infusion, the CIR was greatly reduced (by mean 70.2% of control), but pressor responses from the dorsal medulla were unaffected. In contrast, lesions of greater size placed in the ventrolateral medulla more caudally did not significantly alter resting MAP and only slightly reduced the CIR (by mean 17.0% of control). Vasomotor responses to stimulation of the ventrolateral pressor area were unaffected by caudal ventrolateral lesions, but greatly reduced by dorsomedial lesions in the same plane. It is concluded that the ventrolateral area is either the site of origin or an essential part of the central vasomotor pathway mediating the CIR and that this pathway projects dorsomedially before descending to the spinal cord.

Involvement of the ventrolateral medulla in the mediation of pressor responses of the rat to afferent vagal stimulation

1985 ◽  
Vol 63 (12) ◽  
pp. 1612-1614 ◽  
Author(s):  
T. Kubo
Keyword(s):  
Spinal Cord ◽  
Vagal Stimulation ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Vasopressin Antagonist ◽  
Caudal Ventrolateral Medulla ◽  
Pressor Responses ◽  
Electrolytic Lesions ◽  
Afferent Vagal ◽  
Stimulation Of

Electrical stimulation of afferent vagal fibres evoked a pressor response in rats after transection of the spinal cord. The pressor response was accounted for by an increased release of vasopressin because it was abolished by the intravenous injection of a vasopressin antagonist. Bilateral electrolytic lesions at the sites of the caudal ventrolateral medulla markedly reduced the pressor response to afferent vagal stimulation but not that to carotid occlusion. It is concluded that the area of the caudal ventrolateral medulla is involved in mediation of the vasopressin-induced pressor response to afferent vagal stimulation.

Ventrolateral medullary neurons modulate pressor reflex to muscular contraction

1989 ◽  
Vol 257 (5) ◽  
pp. R1154-R1161 ◽  
Author(s):  
R. M. Bauer ◽  
G. A. Iwamoto ◽  
T. G. Waldrop
Keyword(s):  
Arterial Pressure ◽  
Excitatory Amino Acid ◽  
Pressor Response ◽  
Minute Ventilation ◽  
Muscular Contraction ◽  
Posterior Hypothalamus ◽  
Ventrolateral Medulla ◽  
Pressor Reflex ◽  
Stimulation Of

Cardiorespiratory alterations during exercise are mediated through feedback from contracting muscles and descending drive from rostral brain sites such as the posterior hypothalamus. The role of medullary sites, which process this information, was examined in this study. In anesthetized cats, muscular contraction elicited by stimulation of L7 and S1 ventral roots and electrical stimulation of sites in the posterior hypothalamus both evoked increases in arterial pressure, heart rate, and minute ventilation. The reflex increase in arterial pressure produced by muscular contraction was attenuated significantly 15-20 min after bilateral microinjections of an excitatory amino acid (EAA) receptor antagonist, kynurenic acid (KYN), into the ventrolateral medulla (VLM). The reflex increase in arterial pressure evoked by muscular contraction returned to control levels 90 min after VLM microinjections of KYN. Microinjection of KYN into the VLM had no effect on the cardiorespiratory responses to posterior hypothalamic stimulation. These findings suggest that neurons in the VLM modulate the reflex pressor response evoked by muscular contraction. This reflex may be mediated through an interaction with EAA receptors on neurons in the VLM.

Sympathoexcitatory CVLM neurons mediate responses to caudal pressor area stimulation

2000 ◽  
Vol 279 (2) ◽  
pp. R364-R374 ◽  
Author(s):  
Madhusudan Natarajan ◽  
Shaun F. Morrison
Keyword(s):  
Arterial Pressure ◽  
Kynurenic Acid ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Homocysteic Acid ◽  
Premotor Neurons ◽  
Caudal Pressor ◽  
Excitatory Responses ◽  
Stimulation Of

Neurons in the caudal pressor area (CPA) are a source of tonic sympathoexcitation that is dependent on activation of cardiovascular sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM). In the present study, we sought to clarify the mechanism through which CPA neurons elicit increases in RVLM neuronal discharge, vasoconstrictor sympathetic tone, and arterial pressure. In urethan-chloralose-anesthetized, paralyzed, and artificially ventilated rats, bilateral disinhibition of CPA with bicuculline (Bic) after bilateral disinhibition of caudal ventrolateral medulla (CVLM) caused increases in splanchnic sympathetic nerve activity (+277% control) and arterial pressure (+54 mmHg). Inhibition of CVLM neurons with muscimol abolished the pressor response to activation of CPA neurons, suggesting that neurons within CVLM mediate the excitatory responses from CPA. Disinhibition of CVLM and CPA with Bic enhanced the sympathoexcitatory responses to stimulation of CPA with dl-homocysteic acid, which were blocked by microinjections of kynurenic acid into CVLM. We conclude that the pathway from CPA to RVLM involves an obligatory glutamatergic activation of sympathoexcitatory neurons in the vicinity of CVLM.

Analysis of systemic and pulmonary vascular responses to PACAP and VIP: role of adrenal catecholamines

1992 ◽  
Vol 263 (6) ◽  
pp. H1659-H1669 ◽  
Author(s):  
R. K. Minkes ◽  
T. J. McMahon ◽  
T. R. Higuera ◽  
W. A. Murphy ◽  
D. H. Coy ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Venous Pressure ◽  
Vascular Responses ◽  
Intravenous Injections ◽  
Pressor Responses ◽  
Pituitary Adenylate Cyclase ◽  
Pulmonary Arterial ◽  
Dose Dependent

Systemic and pulmonary vascular responses to pituitary adenylate cyclase-activating polypeptide (PACAP), a novel peptide with 68% sequence homology to vasoactive intestinal peptide (VIP), were investigated in the anesthetized cat. Intravenous injections of PACAP in doses of 0.1–3.0 nmol/kg produced decreases in arterial pressure (AP) at low doses and biphasic changes (decreases followed by increases) at higher doses, which were accompanied by increases in central venous pressure (CVP) and cardiac output (CO), and decreases and biphasic changes in systemic vascular resistance (SVR). In contrast, VIP in doses of 0.1-3.0 nmol/kg produced only dose-dependent decreases in AP and SVR and produced little change in CVP and CO. PACAP produced increased pulmonary arterial pressure (PAP), left atrial pressure (LAP), and increases in pulmonary vascular resistance (PVR). PACAP increased heart rate (HR) and right ventricular contractile force (RVCF), while VIP had no effect. Increases in AP and SVR in response to PACAP were changed to decreases following the administration of phentolamine or after adrenalectomy. Under constant flow conditions, PACAP and VIP produced dose-dependent decreases in lobar arterial pressure when tone was elevated, with PACAP being threefold more potent than VIP. Meclofenamate and nitro-L-arginine methyl ester (L-NAME) had no effect on pulmonary responses to the peptides. PACAP produced dose-dependent biphasic changes in hindquarters perfusion pressure, whereas VIP produced only decreases that were unchanged by indomethacin, L-NAME, and glibenclamide. Phentolamine and adrenalectomy eliminated the hindquarters pressor response to PACAP and D-Phe2-VIP, a VIP antagonist, reduced responses to VIP but not to PACAP. These data suggest that responses to PACAP and VIP are mediated by distinct receptors and that pressor responses to PACAP are due to the release of catecholamines from the adrenal gland.

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