Pressor responses from electrical or glutamate stimulations of the dorsal or ventrolateral medulla

1988 ◽  
Vol 255 (5) ◽  
pp. R709-R717 ◽  
Author(s):  
C. Y. Chai ◽  
R. H. Lin ◽  
A. M. Lin ◽  
C. M. Pan ◽  
E. H. Lee ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Pressor Response ◽  
Monosodium Glutamate ◽  
Pressure Rise ◽  
Ventrolateral Medulla ◽  
Induced Response ◽  
Pressor Responses ◽  
Dorsal Portion ◽  
Caudal Medulla ◽  
Alpha Chloralose

In rats, rabbits, and cats anesthetized with alpha-chloralose and urethan, responses of the pressor areas of the dorsal portion (DM) and ventrolateral portion (VLM) of medulla and pons were compared. Electrical stimulation (monopolar square-wave pulses) on monosodium glutamate solution (Glu, 100-200 nl, 1 M) was delivered through an electrode-needle tubing connected to a Hamilton syringe for semimicroinjection. In all three of these species, pressor responses were elicited from both DM and VLM by either Glu or electrical stimulation. The most active parts of DM were found in the dorsomedial reticular formation of the rostral medulla to mid-medulla. In the pons and caudal medulla, the Glu-induced response was mild, although the electrically induced response was marked. Application of kainic acid (KA) to either DM or VLM produced an initial pressor response but was followed by a reduction of the pressure rise on subsequent electrical stimulation. Glu, unlike electrical stimulation, excites neural perikarya, not fibers of passage. KA initially excites the neural perikarya before causing damage that spares axons. These results thus suggest that both DM and VLM contain neural perikarya that mediate pressor effects.

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.

Glutamatergic and GABAergic inputs to the RVL mediate cardiovascular adjustments to noxious stimulation

2001 ◽  
Vol 280 (2) ◽  
pp. R434-R440 ◽  
Author(s):  
Olga S. Possas ◽  
Oswaldo U. Lopes ◽  
Sérgio L. Cravo
Keyword(s):  
Blood Flow ◽  
Pressor Response ◽  
Muscle Afferents ◽  
Ventrolateral Medulla ◽  
Noxious Stimulation ◽  
Glutamatergic Synapses ◽  
Pressor Responses ◽  
Gabaergic Synapses ◽  
Sciatic Nerve Stimulation

Stimulation of cutaneous and muscle afferents induces several cardiovascular adjustments such as hypertension, tachycardia, and muscle vasodilation. Although previous studies have demonstrated that the rostral ventrolateral medulla (RVL) mediates sympathoexcitation and pressor responses to sciatic nerve stimulation (SNS), whether it also mediates blood flow adjustments remains unclear. Therefore, in the present study, we examined the role of the RVL in the vasodilation induced by SNS and the possible neurotransmitters involved. In Urethane-anesthetized, paralyzed, and artificially ventilated rats, SNS (square pulses, 1 ms, 20 Hz, 800–1200 μA, 10 s) produced increases in blood pressure, heart rate, blood flow, and vascular conductance of the stimulated limb. Unilateral microinjection of kainic acid (2 nmol/100 nl) into the RVL contralateral to the stimulated limb abolished cardiovascular adjustments to SNS. Unilateral microinjections of kynurenic acid (2 nmol/100 nl) selectively abolished the pressor response to SNS, whereas bicuculline (400 pmol/100 nl) abolished the increases in blood flow without changing the pressor response. These results suggest that glutamatergic synapses within the RVL mediate pressor responses, whereas GABAergic synapses may mediate the vasodilation to SNS.

Neurons of C1 area mediate cardiovascular responses initiated from ventral medullary surface

1986 ◽  
Vol 250 (5) ◽  
pp. R932-R945 ◽  
Author(s):  
E. E. Benarroch ◽  
A. R. Granata ◽  
D. A. Ruggiero ◽  
D. H. Park ◽  
D. J. Reis
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Ventral Surface ◽  
Aminobutyric Acid ◽  
Ventrolateral Medulla ◽  
Gamma Aminobutyric Acid ◽  
Pressor Responses ◽  
Ventral Medullary Surface

We sought to establish whether neurons of the C1 area of the rostral ventrolateral medulla (RVL) mediate changes in arterial pressure and heart rate evoked by topical application of drugs to the ventral medullary surface of the rat. Animals were anesthetized, paralyzed, and ventilated. The ventral surface was mapped with L-glutamate, and a restricted zone was identified from which L-glutamate, as well as kainic acid, bicuculline, strychnine, carbachol, or physostigmine, increased arterial pressure and heart rate. The hypertensive effects of carbachol and physostigmine were blocked by previous local application of atropine but not hexamethonium. Application of gamma-aminobutyric acid (GABA) or glycine to this area produced hypotension and bradycardia. Located caudal to the trapezoid bodies and lateral to the pyramids, this area corresponded to points with lowest threshold for pressor responses evoked by electrical stimulation and overlapped the distribution of epinephrine-synthesizing cells of the RVL. Processes arising from these neurons were identified reaching and contacting the ventral surface. Unilateral lesions involving the C1 area or phenylethanolamine-N-methyltransferase-labeled descending axons derived from this area imparied by greater than 70% the response to ipsilateral application of L-glutamate, GABA, or glycine to the ventral surface. We suggest that neurons within the C1 area of RVL adjacent to or including epinephrine cells may mediate cardiovascular changes elicited from a restricted chemosensitive zone of the ventral medullary surface of the rat.

Mechanisms of hemodynamic responses to electrical stimulation of subfornical organ

1986 ◽  
Vol 250 (6) ◽  
pp. R1117-R1122 ◽  
Author(s):  
M. L. Mangiapane ◽  
M. J. Brody
Keyword(s):  
Electrical Stimulation ◽  
Pressor Response ◽  
Subfornical Organ ◽  
Constant Current ◽  
Pulsed Doppler ◽  
Mesenteric Circulation ◽  
Pressor Responses ◽  
Constant Current Stimulation ◽  
Vascular Beds ◽  
Stimulation Of

The rat subfornical organ (SFO) is involved in the pressor response to circulating angiotensin II, and recent evidence indicates that SFO electrical stimulation also produces a pressor response. In the present experiments we examined the hemodynamic, neural, and humoral mechanisms that underlie the pressor response to electrical stimulation of the SFO. Rats were anesthetized with urethan and instrumented with femoral arterial catheters and with pulsed Doppler flow probes on the superior mesenteric and renal arteries and on the abdominal aorta. Constant-current stimulation, delivered to the SFO via tungsten microelectrodes, resulted in stimulus-locked frequency-dependent pressor responses and vasoconstriction in all vascular beds tested. The stimulation-evoked increases in vascular resistance were greatest in the mesenteric circulation and least in the renal. Movement of the electrode away from the SFO produced significantly smaller responses. Ganglionic blockade abolished the responses to electrical stimulation, whereas vasopressin blockade significantly attenuated the responses. The responses of baroreceptor-denervated rats were qualitatively similar to but approximately double in magnitude of those of normal rats. We conclude that electrical stimulation of the SFO elicits widespread regional vasoconstriction that is most pronounced in the mesenteric circulation. The sympathetic nervous system appears responsible for these effects, but there may be facilitation of the responses by vasopressin.

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.

Midbrain central gray: influence on medullary sympathoexcitatory neurons and the baroreflex in rats

1992 ◽  
Vol 263 (1) ◽  
pp. R24-R33 ◽  
Author(s):  
A. J. Verberne ◽  
P. G. Guyenet
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Nerves ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Central Gray ◽  
Train Stimulation ◽  
Pulse Stimulation ◽  
Site Of Stimulation ◽  
Stimulation Of

The influence of the central gray (CG) of the midbrain on the activity of 19 barosensitive sympathoexcitatory neurons of the rostral ventrolateral medulla (RVLM) and on the sympathetic vasomotor baroreflex was studied in halothane-anesthetized rats. Eighteen RVLM barosensitive units were readily activated by train stimulation of the CG, although twin-pulse stimulation was less effective (10 of 19 neurons responded). Inhibition of neurons within the RVLM by bilateral microinjection of the GABA-mimetic drug muscimol abolished the pressor responses to CG stimulation, while the accompanying lumbar nerve sympathoexcitation was converted to sympathoinhibition. In baroreceptor-denervated vagotomized animals, unilateral microinjection of muscimol into the RVLM ipsilateral or contralateral to the site of CG stimulation resulted in approximately equal attenuation of the CG sympathoexcitatory and pressor responses. In contrast, the sympathoexcitatory response to electrical stimulation of the sciatic nerve was reduced more effectively by inhibition of the RVLM contralateral to the site of stimulation. Electrical stimulation of the CG lateral and ventrolateral to the aqueduct produced sympathoexcitation [increased discharge of the greater splanchnic and lumbar sympathetic nerves (SSN and LSN)] with an increase in mean arterial blood pressure. Activation of the SSN by CG stimulation was greater than that observed for the LSN (n = 5 rats). This differential influence of the CG on the sympathetic outflow was not a result of a differential influence of the baroreflex. Electrical stimulation of the CG produced elevations of the gain and the cut-off pressure of the baroreflex for both the SSN and LSN.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebellar pressor response in the dog

1976 ◽  
Vol 41 (4) ◽  
pp. 574-580 ◽  
Author(s):  
K. J. Dormer ◽  
H. L. Stone
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Pressure Rise ◽  
Sympathetic Activation ◽  
Intensity Curve ◽  
Baroreceptor Reflexes ◽  
Mongrel Dog ◽  
Bilateral Vagotomy ◽  
Alpha Chloralose

A fastigial pressor response has been elicited in the anesthetized mongrel dog. Stimulation within the rostral portions of this nucleus results in mean arterial pressure rises up to 150 mmHg above control. A proportional tachycardia is simultaneously evoked which may rapidly attain heart rates of190 beats/min above control levels. Peak tachycardias immediately suside and often the heart rate declines below control values during stimulation while arterial pressure remains elevated. When either the carotid sinuses wereisolated by ligation or a bilateral vagotomy was performed, the fastigial tachycardia was sustained. Thresholds for the response are near 0.05 mA and the stimulus intensity curve is linear to 0.4 mA whereupon the pressure rise and tachycardia begin to approach a plateau value. The response could still be attained when submaximal doses of alpha-chloralose anesthesia or highlevels of barbiturates (30–40 mg/kg) were given. Both portions of the response result from widespread sympathetic activation; however, buffering of the response through the baroreceptor reflexes is only demonstrated in the cardiac segment of the response.

Dietary salt intake alters cardiovascular responses evoked from the rostral ventrolateral medulla

1999 ◽  
Vol 276 (6) ◽  
pp. R1600-R1607 ◽  
Author(s):  
Satoru Ito ◽  
Frank J. Gordon ◽  
Alan F. Sved
Keyword(s):  
Vascular Reactivity ◽  
Salt Intake ◽  
Pressor Response ◽  
Control Diet ◽  
Cardiovascular Responses ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
Pressor Responses

The present experiments examined whether in rats consuming diets with either high NaCl content (8%) or low Na+ content (0.01%) for 2 wk excitatory inputs to the rostral ventrolateral medulla (RVLM) would be altered. In chloralose-anesthetized rats, injection of glutamate into the RVLM elicited a pressor response that, compared with rats fed a control diet, was 50% larger in rats fed a diet containing 8% NaCl and was 25% smaller in rats fed a diet containing 0.01% Na+. Pressor responses produced by electrical stimulation of sciatic nerve afferents, as well as by microinjections into the RVLM ofl-dihydroxyphenylalanine or carbachol, were all potentiated by high dietary salt intake and reduced by low dietary salt intake. Dietary salt intake had no effect on pressor responses produced by intravenous injection of phenylephrine, indicating that salt-related alterations in cardiovascular responses produced by central activation could not be accounted for by changes in peripheral vascular reactivity. The decrease in arterial pressure produced by injection of glutamate into the nucleus of the solitary tract was also potentiated by the high salt diet, suggesting that the sensitivity of central baroreceptor reflex pathways may be altered by dietary NaCl. These results indicate that the amount of NaCl consumed in the diet can change the sensitivity of RVLM sympathoexcitatory neurons, and this change in sensitivity is not restricted to any particular class of cell surface receptors.

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