Inhibition of baroreflex vagal bradycardia by activation of the rostral ventrolateral medulla in rats

2000 ◽  
Vol 279 (3) ◽  
pp. H1239-H1247 ◽  
Author(s):  
Shoichiro Nosaka ◽  
Keiko Murata ◽  
Masayoshi Kobayashi ◽  
Zhi Bin Cheng ◽  
Junko Maruyama
Keyword(s):  
Blood Pressure ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Inhibitory Influence ◽  
Homocysteic Acid ◽  
Aortic Depressor Nerve ◽  
Inspiratory Activity ◽  
Gaba Antagonist ◽  
Vagal Bradycardia

In stressful conditions, baroreflex vagal bradycardia (BVB) is often suppressed while blood pressure is increased. To address the role of the rostral ventrolateral medulla (RVL), a principal source of sympathetic tone, in inhibition of BVB, we microinjected dl-homocysteic acid (DLH, 6 nmol) into the RVL of chloralose-urethan-anesthetized, sinoaortic-denervated rats to examine the effect on BVB. The BVB was provoked by electrical stimulation of the aortic depressor nerve ipsilateral to the injection sites. DLH microinjection was found to suppress BVB while increasing blood pressure. The inhibition of BVB was observed even during the early phase in which DLH transiently suppressed central inspiratory activity. The inhibition was not affected either by upper spinal cord transection or suprapontine decerebration. Similar results were obtained by microinjection of bicuculline methiodide (160 pmol), a GABA antagonist, into the RVL of carotid sinus nerve-preserved rats due to withdrawal of a tonic GABA-mediated, inhibitory influence including the input from arterial baroreceptors. In conclusion, activation of the RVL inhibits BVB at brain stem level independently of central inspiratory drive.

GABAergic responses in ventrolateral medulla in spontaneously hypertensive rats

1990 ◽  
Vol 258 (2) ◽  
pp. R450-R456 ◽  
Author(s):  
J. K. Smith ◽  
K. W. Barron
Keyword(s):  
Ventral Surface ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Gamma Aminobutyric Acid ◽  
Spontaneously Hypertensive ◽  
Sh Group ◽  
Gaba Antagonist ◽  
Wistar Kyoto ◽  
The Brain

Gamma-Aminobutyric acid (GABA) and the GABA antagonist bicuculline methiodide were used to investigate the role of GABAergic transmission in the rostral and caudal ventrolateral medulla in 12- to 13-wk-old spontaneously hypertensive (SH) (n = 7) and normotensive, control Wistar-Kyoto (WKY) (n = 7) rats. Animals were anesthetized with urethan (1.25 g/kg sc), paralyzed with gallamine triethiodide (10 mg/kg iv), and artificially ventilated. Femoral arterial and venous catheters were inserted for the measurement of mean arterial pressure (MAP) and heart rate responses and for intravenous infusions. The ventral surface of the brain stem then was exposed. The responsiveness of the rostral ventrolateral medulla to GABA was compared in SH and WKY rats using unilateral microinjections (30 nl) of GABA at 1, 10, and 100 mM concentrations, which produced significantly (P less than 0.05) larger decreases of MAP in SH rats compared with WKY at the 10 and 100 mM concentrations (-37.3 +/- 2.8 mmHg for SH vs. -27.3 +/- 2.7 mmHg for WKY at 100 mM). Tonic GABAergic inhibition was gauged using bilateral microinjections (30 nl) of bicuculline (2 and 4 mM) into the rostral ventrolateral medulla, which caused significantly larger increases in MAP in the WKY group (+84.8 +/- 8.5 mmHg at 4 mM) compared with the SH group (+14.9 +/- 5.8 mmHg at 4 mM). In contrast, the ability to drive sympathetic outflow by microinjection of L-glutamate in the rostral ventrolateral medulla was not significantly different between WKY and SH rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of the Rostral Ventrolateral Medulla in Maintenance of Blood Pressure in Rats With Goldblatt Hypertension

Hypertension ◽  
1995 ◽  
Vol 26 (6) ◽  
pp. 1117-1120 ◽  
Author(s):  
Cassia Bergamaschi ◽  
Ruy R. Campos ◽  
Nestor Schor ◽  
Oswaldo U. Lopes
Keyword(s):  
Blood Pressure ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Goldblatt Hypertension

Midbrain vlPAG inhibits rVLM cardiovascular sympathoexcitatory responses during electroacupuncture

2006 ◽  
Vol 290 (6) ◽  
pp. H2543-H2553 ◽  
Author(s):  
Stephanie C. Tjen-A-Looi ◽  
Peng Li ◽  
John C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Excitatory Amino Acid ◽  
Sympathetic Neurons ◽  
Cardiovascular Responses ◽  
Splanchnic Nerve ◽  
Ventrolateral Medulla ◽  
Inhibitory Influence ◽  
Afferent Stimulation ◽  
Homocysteic Acid ◽  
Blood Pressure Responses

The periaqueductal gray (PAG) is an important integrative region in the regulation of autonomic outflow and cardiovascular function and may serve as a regulatory center as part of a long-loop pathway during somatic afferent stimulation with acupuncture. Because the ventrolateral PAG (vlPAG) provides input to the rostral ventrolateral medulla (rVLM), an important area for electroacupuncture (EA) regulation of sympathetic outflow, we hypothesized that the vlPAG plays a role in the EA-related modulation of rVLM premotor sympathetic neurons activated during visceral afferent stimulation and autonomic excitatory reflexes. Cats were anesthetized and ventilated, and heart rate and mean blood pressure were monitored. Stimulation of the splanchnic nerve by a pledget of filter paper soaked in bradykinin (BK, 10 μg/ml) every 10 min on the gallbladder induced consistent cardiovascular reflex responses. Bilateral stimulation with EA at acupoints over the pericardial meridian (P5-6) situated over the median nerve reduced the increases in blood pressure from 34 ± 3 to 18 ± 5 mmHg for a period of time that lasted for 60 min or more. Unilateral inactivation of neuronal activity in the vlPAG with 50–75 nl of kainic acid (KA, 1 mM) restored the blood pressure responses from 18 ± 3 to 36 ± 5 mmHg during BK-induced gallbladder stimulation, an effect that lasted for 30 min. In the absence of EA, unilateral microinjection of the excitatory amino acid dl-homocysteic acid (DLH, 4 nM) in the vlPAG mimicked the effect of EA and reduced the reflex blood pressure responses from 35 ± 6 to 14 ± 5 mmHg. Responses of 21 cardiovascular sympathoexcitatory rVLM neurons, including 12 that were identified as premotor neurons, paralleled the cardiovascular responses. Thus splanchnic nerve-evoked neuronal discharge of 32 ± 4 spikes/30 stimuli in six neurons was reduced to 10 ± 2 spikes/30 stimuli by EA, which was restored rapidly to 28 ± 4 spikes/30 stimuli by unilateral injection of 50 nl KA into the vlPAG. Conversely, 50 nl of DLH in the vlPAG reduced the number of action potentials of 5 rVLM neurons from 30 ± 4 to 18 ± 4 spikes/30 stimuli. We conclude that the inhibitory influence of EA involves vlPAG stimulation, which, in turn, inhibits rVLM neurons in the EA-related attenuation of the cardiovascular excitatory response during visceral afferent stimulation.

Lack of involvement of GABA in baroreceptor-mediated sympathoinhibition

1986 ◽  
Vol 250 (6) ◽  
pp. R1065-R1073 ◽  
Author(s):  
R. B. McCall
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Gamma Aminobutyric Acid ◽  
Gaba Antagonists ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Nerve Discharge

The purpose of the present investigation was to determine if gamma-aminobutyric acid (GABA) mediates the baroreceptor-induced inhibition of sympathetic nerve discharge (SND) in dialurethan-anesthetized cats. The GABA antagonists picrotoxin and bicuculline produced marked elevations in arterial blood pressure and inferior cardiac SND. The inhibition of SND observed during pressor responses was occasionally slightly depressed after picrotoxin or bicuculline. Midcollicullar transection blocked or reversed the increase in blood pressure and SND produced by GABA antagonists. Under these conditions, baroreceptor inhibition of SND was not affected by picrotoxin. Microinjections of picrotoxin into the rostral ventrolateral medulla produced increases in arterial blood pressure and SND but failed to affect baroreceptor-induced sympathoinhibition. GABA antagonists given intravenously also failed to affect the baroreceptor-induced inhibition of sympathetically related neurons recorded in the rostral ventrolateral medulla. However, intravenous picrotoxin did antagonize the inhibitory affect of microiontophoretically applied GABA on these neurons. These data provide no evidence to support the contention that GABA mediates the baroreceptor-induced inhibition of SND. The role of GABA in regulating SND is discussed.

Blockade of angiotensin receptors in rat rostral ventrolateral medulla removes excitatory vasomotor tone

1996 ◽  
Vol 270 (6) ◽  
pp. R1317-R1323 ◽  
Author(s):  
S. Ito ◽  
A. F. Sved
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Angiotensin Receptors ◽  
Inhibitory Influence ◽  
Primary Role ◽  
Arterial Blood ◽  
Local Injections ◽  
Stimulation Of

The rostral ventrolateral medulla (RVLM) plays a primary role in the tonic and phasic control of arterial blood pressure. Stimulation of angiotensin receptors in this region appears to contribute to the tonic excitatory drive of RVLM neurons involved in the control of blood pressure, but the extent of this contribution has not been previously evaluated. The present study used bilateral microinjections of angiotensin receptor antagonists into the RVLM of chloralose-anesthetized rats to determine the degree to which tonic blood pressure was dependent upon this angiotensin-mediated input. Bilateral injection into the RVLM of 1 nmol of [Sar1, Thr8]angiotensin II or [Sar1, Ile8] angiotensin II decreased blood pressure approximately 40 mmHg. The decrease in blood pressure elicited by these angiotensin antagonists was nearly as great as that elicited by complete bilateral inhibition of the RVLM produced by local injections of muscimol or elicited by inhibition of the autonomic nervous system by intravenous injection of chlorisondamine. The decrease in blood pressure caused by injection of these angiotensin antagonists was localized to the RVLM and was dose related. Responses elicited by [Sar1, Thr8]angiotensin II were eliminated by coinjection of angiotensin. In addition to markedly decreasing resting blood pressure, 1 nmol of [Sar1, Thr8]angiotensin II injected into the RVLM, also completely antagonized the increase in blood pressure elicited by blocking the tonic inhibitory influence exerted on the RVLM by neurons in the caudal ventrolateral medulla. These results demonstrate that tonic stimulation of angiotensin receptors in the RVLM accounts for much of the excitatory sympathetic vasomotor drive emanating from the RVLM.

The role of the rostral ventrolateral medulla in systolic blood pressure frequency content within the Mayer wave band

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Cecilia Badenhorst ◽  
Jordan W. Squair ◽  
Matthieu Gautier ◽  
Jan Elaine Soriano ◽  
Gregoire Courtine ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Wave Band ◽  
Frequency Content ◽  
Mayer Wave

Vasomotor control by subretrofacial neurones in the rostral ventrolateral medulla

1987 ◽  
Vol 65 (8) ◽  
pp. 1572-1579 ◽  
Author(s):  
R. A. L. Dampney ◽  
A. K. Goodchild ◽  
R. M. McAllen
Keyword(s):  
Blood Pressure ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Unit Recording ◽  
Sympathetic Vasoconstriction ◽  
Afferent Inputs ◽  
Retrofacial Nucleus ◽  
P Cells ◽  
Bilateral Destruction

In this paper we review our recent work in the rabbit and cat on the role of the rostral ventrolateral medulla in cardiovascular regulation. Microinjection of neuroexcitatory amino acids into a highly circumscribed region, located just ventral to the retrofacial nucleus at the level of the rostral part of the inferior olive, leads to an increase in blood pressure, owing to sympathetic vasoconstriction. Bilateral destruction of this region, which we have termed the subretrofacial nucleus, leads to a profound fall in blood pressure. Anatomical studies show that the subretrofacial nucleus contains a compact group of bulbospinal neurones that project to sympathetic preganglionic nuclei in the thoracolumbar spinal cord. Single-unit recording studies have shown that these bulbospinal neurons are spontaneously active and are powerfully inhibited by baroreceptor inputs. These observations indicate that the subretrofacial bulbospinal cells are sympathoexcitatory and play a major role in the tonic and phasic control of the cardiovascular system. Some important unresolved questions regarding the subretrofacial neurones will be discussed. (i) Are they functionally homogeneous, or are they viscerotopically organized with respect to particular end organs? (ii) What are their afferent inputs? (iii) What are their histochemical properties? Specifically, are they part of the group of adrenaline-synthesizing cells, or alternatively, substance P cells?

Cardiac baroreflex facilitation evoked by hypothalamus and prefrontal cortex stimulation: role of the nucleus tractus solitarius 5-HT2A receptors

2006 ◽  
Vol 291 (4) ◽  
pp. R1007-R1015 ◽  
Author(s):  
C. Sévoz-Couche ◽  
M. A. Comet ◽  
J. F. Bernard ◽  
M. Hamon ◽  
R. Laguzzi
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Prefrontal Cortex ◽  
Nucleus Tractus Solitarius ◽  
Cardiovascular Responses ◽  
Receptor Activation ◽  
Cardiac Response ◽  
Inhibitory Influence ◽  
Homocysteic Acid

We previously showed that serotonin (5-HT2) receptor activation in the nucleus of the tractus solitarius (NTS) produced hypotension, bradycardia, and facilitation of the baroreflex bradycardia. Activation of the preoptic area (POA) of the hypothalamus, which is involved in shock-evoked passive behaviors, induces similar modifications. In addition, previous studies showed that blockade of the infralimbic (IL) part of the medial prefrontal cortex, which sends projections to POA, produced an inhibitory influence on the baroreflex cardiac response. Thus, to assess the possible implication of NTS 5-HT2 receptors in passive cardiovascular responses, we analyzed in anesthetized rats the effects of NTS inhibition and NTS 5-HT2 receptor blockade on the cardiovascular modifications induced by chemical (0.3 M d,l-homocysteic acid) and electrical (50 Hz, 150–200 μA) stimulation of IL or POA. Intra-NTS microinjections of muscimol, a GABAA receptor agonist, prevented the decreases in blood pressure and heart rate normally evoked by IL or POA activation. In addition, we found that intra-NTS microinjection of R(+)-α-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidine-methanol, a specific 5-HT2A receptor antagonist, did not affect the decreases in cardiovascular baseline parameters induced by IL or POA stimulation but prevented the facilitation of the aortic baroreflex bradycardia normally observed during IL (+65 and +60%) or POA (+70 and +69%) electrical and chemical stimulation, respectively. These results show that NTS 5-HT2A receptors play a key role in the enhancement of the cardiac response of the baroreflex but not in the changes in basal heart rate and blood pressure induced by IL or POA stimulation.

scholarly journals Serotonergic projection from nucleus raphe pallidus to rostral ventrolateral medulla modulates cardiovascular reflex responses during acupuncture

2010 ◽  
Vol 108 (5) ◽  
pp. 1336-1346 ◽  
Author(s):  
Ali Moazzami ◽  
Stephanie C. Tjen-A-Looi ◽  
Zhi-Ling Guo ◽  
John C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Rostral Ventrolateral Medulla ◽  
Reflex Response ◽  
Ventrolateral Medulla ◽  
Serotonergic Neurons ◽  
Homocysteic Acid ◽  
Reflex Responses ◽  
Cardiovascular Reflex ◽  
Raphe Pallidus ◽  
Stimulation Of

We have demonstrated that stimulation of somatic afferents during electroacupuncture (EA) inhibits sympathoexcitatory cardiovascular rostral ventrolateral medulla (rVLM) neurons and reflex responses. Furthermore, EA at P5-P6 acupoints over the median nerve on the forelimb activate serotonin (5-HT)-containing neurons in the nucleus raphe pallidus (NRP). The present study, therefore, examined the role of the NRP and its synaptic input to neurons in the rVLM during the modulatory influence of EA. Since serotonergic neurons in the NRP project to the rVLM, we hypothesized that the NRP facilitates EA inhibition of the cardiovascular sympathoexcitatory reflex response through activation of 5-HT1Areceptors in the rVLM. Animals were anesthetized and ventilated, and heart rate and blood pressure were monitored. We then inserted microinjection and recording electrodes in the rVLM and NRP. Application of bradykinin (10 μg/ml) on the gallbladder every 10 min induced consistent excitatory cardiovascular reflex responses. Stimulation with EA at P5-P6 acupoints reduced the increase in blood pressure from 41 ± 4 to 22 ± 4 mmHg for more than 70 min. Inactivation of NRP with 50 nl of kainic acid (1 mM) reversed the EA-related inhibition of the cardiovascular reflex response. Similarly, blockade of 5-HT1Areceptors with the antagonist WAY-100635 (1 mM, 75 nl) microinjected into the rVLM reversed the EA-evoked inhibition. In the absence of EA, NRP microinjection of dl-homocysteic acid (4 nM, 50 nl), to mimic EA, reduced the cardiovascular and rVLM neuronal excitatory reflex response during stimulation of the gallbladder and splanchnic nerve, respectively. Blockade of 5-HT1Areceptors in the rVLM reversed the NRP dl-homocysteic acid inhibition of the cardiovascular and neuronal reflex responses. Thus activation of the NRP, through a mechanism involving serotonergic neurons and 5-HT1Areceptors in the rVLM during somatic stimulation with EA, attenuates sympathoexcitatory cardiovascular reflexes.

Sign in / Sign up

Export Citation Format

Share Document