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.

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.

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.

Neurons of rostral ventrolateral medulla mediate somatic pressor reflex

1989 ◽  
Vol 256 (2) ◽  
pp. R448-R462 ◽  
Author(s):  
R. L. Stornetta ◽  
S. F. Morrison ◽  
D. A. Ruggiero ◽  
D. J. Reis
Keyword(s):  
Spinal Cord ◽  
Kainic Acid ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Reticular Nucleus ◽  
Lumbar Spinal Cord ◽  
Afferent Nerves ◽  
Electrolytic Lesions ◽  
Pressor Reflex ◽  
Stimulation Of

The somatic pressor reflex (SPR) elicited in anesthetized paralyzed rats by electrical stimulation of the sciatic or sural cutaneous afferent nerves produced an increase in arterial pressure ranging from 5 to 40 mmHg. Stimulation of femoral or tibial afferent nerves from muscle produced a depressor response. The SPR was not affected by midpontine transection but was eliminated either by hemisection of the lumbar spinal cord contralateral, but not ipsilateral, to the stimulated nerve or by electrolytic or kainic acid lesion of the contralateral, but not ipsilateral, rostral ventrolateral medulla (RVL). Stimulation of the brachial plexus elicited an SPR that was not eliminated by contralateral lumbar hemisection but was abolished by RVL lesion. RVL lesions consistently overlapped areas containing phenylethanolamine N-methyltransferase-labeled C1 adrenergic neurons. Kainic acid injections into the lateral reticular nucleus (LRN) did not affect the SPR. Neither contralateral nor ipsilateral electrolytic lesions of other autonomic areas including parabrachial nucleus, the nucleus tractus solitarii, the A5 region, or the inferior cerebellar peduncle (output pathway of the LRN) affected the reflex. In axonal transport studies using horseradish peroxidase, afferent terminals of the sciatic nerve were shown to overlap spinoreticular neurons in the dorsal horn retrogradely labeled from tracer injections in the RVL. We conclude that the SPR can be elicited in rats, that it is mediated by spinoreticular afferents traveling in the contralateral spinal cord, and that the C1 adrenergic area of the RVL is a critical region for the integration of the somatic pressor reflex.

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.

Role of ventrolateral medulla in reflex cardiovascular responses to activation of skin and muscle nerves

1995 ◽  
Vol 268 (6) ◽  
pp. R1464-R1471 ◽  
Author(s):  
P. Ruggeri ◽  
R. Ermirio ◽  
C. Molinari ◽  
F. R. Calaresu
Keyword(s):  
Nerve Stimulation ◽  
Sural Nerve ◽  
Tibial Nerve ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Electrolytic Lesions ◽  
Cardiovascular Neurons ◽  
Muscle Nerve ◽  
Stimulation Of

Central neuronal circuits mediating reflex cardiovascular responses to skin and muscle nerve stimulation were studied in rats under urethan anesthesia. Responses of right rostral ventrolateral medulla (RVLM) and caudal ventrolateral medulla (CVLM) cardiovascular neurons to stimulation of contralateral skin and muscle afferent fibers were investigated. Stimulation of the tibial (muscle) nerve excited 19 (86%) of 22 CVLM neurons and inhibited 18 (82%) of 22 RVLM neurons. Stimulation of the sural (skin) nerve excited 20 (91%) of the 22 RVLM neurons but did not affect the firing rate of any of the 22 CVLM neurons. Electrolytic lesions of the CVLM abolished the depressor responses induced by stimulation of the tibial nerve without affecting the pressor response caused by sural nerve stimulation. Similarly, reversible blockade of the CVLM by microinjection of gamma-amino-butyric acid or CoCl2 abolished the depressor response to stimulation of the tibial nerve without affecting the pressor response induced by sural nerve stimulation. These results suggest that vasodepressor responses to muscle nerve activation are mediated by a neuronal inhibitory pathway to the RVLM relayed through the CVLM.

Spinal NMDA receptors mediate pressor responses evoked from the rostral ventrolateral medulla

1991 ◽  
Vol 260 (1) ◽  
pp. H267-H275 ◽  
Author(s):  
M. K. Bazil ◽  
F. J. Gordon
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Nmda Receptors ◽  
Excitatory Amino Acid ◽  
Cardiovascular Responses ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Pressor Responses

These studies investigated the role of spinal N-methyl-D-aspartic acid (NMDA) receptors in the mediation of cardiovascular responses evoked by L-glutamate (L-Glu) stimulation of the rostral ventrolateral medulla (RVM). Microinjections of L-Glu into the RVM of urethan-anesthetized rats increased mean arterial pressure (MAP) and heart rate. Intrathecal administration of the NMDA receptor antagonists D-(-)-2-amino-7-phosphonoheptanoic acid (D-AP-7) or 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonate (CPP) reduced MAP and heart rate. Blockade of NMDA receptors by D-AP-7 or CPP in the caudal thoracic spinal cord markedly reduced RVM pressor responses with little effect on evoked tachycardia. Administration of D-AP-7 to the rostral thoracic spinal cord had no effect on RVM pressor or tachycardic responses. Intrathecal D-AP-7 and CPP abolished the cardiovascular effects of intrathecal NMDA without reducing those produced by intrathecal kainic acid or the quisqualate agonist DL-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA). These results indicate that 1) tonic activation of spinal NMDA receptors participates in the maintenance of sympathetic outflow to the heart and blood vessels, 2) pressor responses evoked from the RVM require synaptic activation of spinal NMDA receptors, and 3) an excitatory amino acid may be the neurotransmitter of pressor pathways descending from the RVM to the spinal cord.

Afferent vagal stimulation, vasopressin, and nitroprusside alter cerebrospinal fluid kinin

1987 ◽  
Vol 253 (1) ◽  
pp. R136-R141 ◽  
Author(s):  
G. R. Thomas ◽  
H. Thibodeaux ◽  
H. S. Margolius ◽  
J. G. Webb ◽  
P. J. Privitera
Keyword(s):  
Cerebrospinal Fluid ◽  
Vagal Stimulation ◽  
Cardiovascular Regulation ◽  
Perfusion System ◽  
Ventriculocisternal Perfusion ◽  
Anesthetized Dogs ◽  
Bilateral Vagotomy ◽  
Afferent Vagal ◽  
Nitroprusside Infusion ◽  
Stimulation Of

The effects of afferent vagal stimulation, cerebroventricular vasopressin, and intravenous nitroprusside on cerebrospinal fluid (CSF) kinin levels, mean arterial pressure (MAP), and heart rate (HR) were determined in anesthetized dogs in which a ventriculocisternal perfusion system (VP) was established. Following bilateral vagotomy, stimulation of the central ends of both vagi for 60 min significantly increased MAP and CSF perfusate levels of kinin and norepinephrine (NE). MAP was increased a maximum of 32 +/- 4 mmHg, and the rates of kinin and NE appearance into the CSF perfusate increased from 4.2 +/- 1.4 to 22.1 +/- 6.9 and from 28 +/- 5 to 256 +/- 39 pg/min, respectively. A significant correlation was found between CSF kinin and NE levels in these experiments. In other experiments the addition of arginine vasopressin to the VP system caused a significant increase in CSF perfusate kinin without affecting MAP or HR. Intravenous infusion of nitroprusside lowered MAP without affecting kinin levels in the CSF. However, on cessation of nitroprusside infusion, CSF kinin increased significantly in association with the return in MAP to predrug level. Collectively the data are consistent with the hypothesis that central nervous system kinins have some role in cardiovascular regulation, and furthermore that this role may involve an interaction between brain kinin and central noradrenergic neuronal pathways.

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