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Rostral Ventrolateral Medulla (rostral + ventrolateral_medulla)

Distribution by Scientific Domains

Life Sciences	52%
Medical Sciences	47%

Distribution within Life Sciences

Neuroscience	44%
Anatomy & Physiology	36%

Selected Abstracts

Direct Evidence for Imidazoline (I1) Receptor Modulation of Ethanol Action on Norepinephrine-Containing Neurons in the Rostral Ventrolateral Medulla in Conscious Spontaneously Hypertensive Rats

ALCOHOLISM, Issue 4 2007
Guichu Li
Background: Enhancement of the rostral ventrolateral medulla (RVLM) presympathetic (norepinephrine, NE) neuronal activity represents a neurochemical mechanism for the pressor effect of ethanol. In this study, we tested the hypothesis that ethanol action on RVLM presympathetic neurons is selectively influenced by the signaling of the local imidazoline (I1) receptor. To support a neuroanatomical and an I1 -signaling selectivity of ethanol, and to circumvent the confounding effects of anesthesia, the dose-related neurochemical and blood pressure effects of ethanol were investigated in the presence of selective pharmacological interventions that cause reduction in the activity of RVLM or nucleus tractus solitarius (NTS) NE neurons via local activation of the I1 or the ,2 -adrenergic receptor in conscious spontaneously hypertensive rats. Results: Local activation of the I1 receptor by rilmenidine (40 nmol) or by the I1/,2 receptor mixed agonist clonidine (1 nmol), and local activation of the ,2 -adrenergic receptor (,2AR) by the pure ,2AR agonist , -methylnorepinephrine (, -MNE, 10 nmol) caused reductions in RVLM NE, and blood pressure. Intra-RVLM ethanol (1, 5, or 10 ,g), microinjected at the nadir of the neurochemical and hypotensive responses, elicited dose-dependent increments in RVLM NE and blood pressure in the presence of local I1,but not ,2 -receptor activation. Only intra-NTS , -MNE, but not rilmenidine or clonidine, elicited reductions in local NE and blood pressure; ethanol failed to elicit any neurochemical or blood pressure responses in the presence of local activation of the ,2AR within the NTS. Conclusion: The findings support the neuroanatomical selectivity of ethanol, and support the hypothesis that the neurochemical (RVLM NE), and the subsequent cardiovascular, effects of ethanol are selectively modulated by I1 receptor signaling in the RVLM. [source]

Reactive oxygen species in rostral ventrolateral medulla modulate cardiac sympathetic afferent reflex in rats

ACTA PHYSIOLOGICA, Issue 4 2009
M.-K. Zhong
Abstract Aim:, The aim of the present study was to investigate whether reactive oxygen species (ROS) in rostral ventrolateral medulla (RVLM) modulate cardiac sympathetic afferent reflex (CSAR) and the enhanced CSAR response caused by microinjection of angiotensin II (Ang II) into the paraventricular nucleus (PVN). Methods:, Under urethane and ,-chloralose anaesthesia, renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) were recorded in sinoaortic-denervated and cervical-vagotomized rats. The CSAR was evaluated by the RSNA response to epicardial application of capsaicin (1.0 nmol). Results:, Bilateral RVLM microinjection of tempol (a superoxide anion scavenger) or polyethylene glycol-superoxide dismutase (PEG-SOD, an analogue of endogenous superoxide dismutase) attenuated the CSAR, but did not cause significant change in baseline RSNA and MAP. NAD(P)H oxidase inhibitors apocynin or phenylarsine oxide (PAO) also showed similar effects, but SOD inhibitor diethyldithio-carbamic acid (DETC) enhanced the CSAR and baseline RSNA, and increased the baseline MAP. Bilateral PVN microinjection of Ang II (0.3 nmol) enhanced the CSAR and increased RSNA and MAP, which was inhibited by the pre-treatment with RVLM administration of tempol, PEG-SOD, apocynin or PAO. The pre-treatment with DETC in the RVLM only showed a tendency in potentiating the CSAR response of Ang II in the PVN, but significantly potentiated the RSNA and MAP responses of Ang II. Conclusion:, These results suggest that the NAD(P)H oxidase-derived ROS in the RVLM modulate the CSAR. The ROS in the RVLM is necessary for the enhanced CSAR response caused by Ang II in the PVN. [source]

C1 neurons in the rat rostral ventrolateral medulla differentially express vesicular monoamine transporter 2 in soma and axonal compartments

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2008
C. P. Sevigny
Abstract Vesicular monoamine transporter 2 (VMAT2) packages biogenic amines into large dense core and synaptic vesicles for either somatodendritic or synaptic release from neurons of the CNS. Whilst the distribution of VMAT2 has been well characterized in many catecholaminergic cell groups, its localization amongst C1 adrenergic neurons in the medulla has not been examined in detail. Within the rostral ventrolateral medulla (RVLM), C1 neurons are a group of barosensitive, adrenergic neurons. Rostral C1 cells project to the thoracic spinal cord and are considered sympathetic premotor neurons. The majority of caudal C1 cells project rostrally to regions such as the hypothalamus. The present study sought to quantitate the somatodendritic expression of VMAT2 in C1 neurons, and to assess the subcellular distribution of the transporter. Immunoreactivity for VMAT2 occurred in 31% of C1 soma, with a high proportion of these in the caudal part of the RVLM. Retrograde tracing studies revealed that only two of 43 bulbospinal C1 neurons contained faint VMAT2-immunoreactivity, whilst 88 ± 5% of rostrally projecting neurons were VMAT2-positive. A lentivirus, designed to express green fluorescent protein exclusively in noradrenergic and adrenergic neurons, was injected into the RVLM to label C1 neurons. Eighty-three percent of C1 efferents that occurred in close proximity to sympathetic preganglionic neurons within the T3 intermediolateral cell column contained VMAT2-immunoreactivity. These data demonstrate differential distribution of VMAT2 within different subpopulations of C1 neurons and suggest that this might reflect differences in somatodendritic vs. synaptic release of catecholamines. [source]

Premotor sympathetic neurons of conditioned fear in the rat

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2008
Pascal Carrive
Abstract Conditioned fear to context, a pure form of psychological stress, is associated with sympathetically mediated changes including a marked hypertension. To identify the possible premotor sympathetic neurons mediating these changes, we conducted double-immunolabelling experiments combining fear-induced Fos with retrograde tracing from the thoracic cord (T2-L1). Presympathetic groups showing the greatest increase in the proportion of spinally projecting cells double-labelled with Fos compared with resting controls were the perifornical area (PeF; 22.7% vs. 0.4%) and paraventricular nucleus (Pa; 10.5% vs. 0.2%) in the hypothalamus, and the A5 noradrenergic group (33.6% vs. 0.2%) in the pons. In contrast, there was only a small increase in the presympathetic groups of the rostral ventral medulla, including the lateral paragigantocellular group (LPGi; 4.3% vs. 0.5%), raphe magnus and pallidus (1.1% vs. 0.6% and 1.8% vs. 0.5%), and the vasopressor group of the rostral ventrolateral medulla (RVLM; 1.9% vs. 0.8%). PeF, Pa, A5 and LPGi accounted for 21, 15, 16 and 6% of all the double-labelled cells, respectively, and RVLM for only 1%. Double-immunolabelling of Fos and tyrosine hydroxylase confirmed that many A5 neurons were activated (19%) and that practically no C1 neurons in RVLM were (1.3%). The results suggest that the main premotor sympathetic drive of the fear response comes from hypothalamic (PeF and Pa) and A5 neurons that project directly to the thoracic cord and bypass medullary presympathetic groups, and that the vasopressor premotor sympathetic neurons of the RVLM are unlikely to mediate the hypertensive pressure response of contextual fear. [source]

Optical imaging of medullary ventral respiratory network during eupnea and gasping In situ

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2006
Jeffrey T. Potts
Abstract In severe hypoxia, respiratory rhythm is shifted from an eupneic, ramp-like motor pattern to gasping characterized by a decrementing pattern of phrenic motor activity. However, it is not known whether hypoxia reconfigures the spatiotemporal organization of the central respiratory rhythm generator. Using the in situ arterially perfused juvenile rat preparation, we investigated whether the shift from eupnea to gasping was associated with a reconfiguration of the spatiotemporal pattern of respiratory neuronal activity in the ventral medullary respiratory network. Optical images of medullary respiratory network activity were obtained from male rats (4,6 weeks of age). Part of the medullary network was stained with a voltage-sensitive dye (di-2 ANEPEQ) centred both within, and adjacent to, the pre-Bötzinger complex (Pre-BötC). During eupnea, optical signals initially increased prior to the onset of phrenic activity and progressively intensified during the inspiratory phase peaking at the end of inspiration. During early expiration, fluorescence was also detected and slowly declined throughout this phase. In contrast, hypoxia shifted the respiratory motor pattern from eupnea to gasping and optical signals were restricted to inspiration only. Areas active during gasping showed fluorescence that was more intensive and covered a larger region of the rostral ventrolateral medulla compared to eupnea. Regions exhibiting peak inspiratory fluorescence did not coincide spatially during eupnea and gasping. Moreover, there was a recruitment of additional medullary regions during gasping that were not active during eupnea. These results provide novel evidence that the shift in respiratory motor pattern from eupnea to gasping appears to be associated with a reconfiguration of the central respiratory rhythm generator characterized by changes in its spatiotemporal organization. [source]

Exposure to a hot environment can activate rostral ventrolateral medulla-projecting neurones in the hypothalamic paraventricular nucleus in conscious rats

EXPERIMENTAL PHYSIOLOGY, Issue 1 2008
Joo Lee Cham
A major integrative site within the brain for autonomic function is the hypothalamic paraventricular nucleus (PVN). Several studies have suggested that the PVN may be involved in the responses regulating body temperature. Hyperthermia elicits redirection of blood flow from the viscera to the periphery and involves changes in sympathetic nerve activity mediated by the central nervous system. The hypothalamic PVN includes neurones that project to the rostral ventrolateral medulla (RVLM), an important autonomic region involved in the tonic regulation of sympathetic nerve activity. This pathway could contribute to the cardiovascular changes induced by hyperthermia. The PVN has a high concentration of nitrergic neurones and it is known that nitric oxide within the brain mediates heat dissipation. Thus the aims of this study were to determine whether RVLM-projecting neurones in the PVN are activated by heat and whether those neurones are also nitrergic. The results show that, compared with control conditions, exposure of conscious rats to a hot environment of 39°C significantly increased the number of neurones containing a Fos-positive nucleus (a marker of activation) and significantly increased the number of activated RVLM-projecting neurones in the PVN. Also, although heating significantly increased the number of activated nitrergic PVN neurones, triple-labelled neurones (i.e. activated, nitrergic and RVLM projecting) in the PVN were rarely observed. The results suggest that RVLM-projecting neurones in the PVN may play a role in responses to heat exposure but these are not nitrergic. [source]

Brain superoxide as a key regulator of the cardiovascular response to emotional stress in rabbits

EXPERIMENTAL PHYSIOLOGY, Issue 3 2007
Dmitry N. Mayorov
Cardiovascular reactivity, an abrupt increase in blood pressure and heart rate in response to emotional stress, is a risk factor for hypertension and heart disease. Brain angiotensin II (Ang II) type 1 (AT1) receptor is increasingly recognized as an important regulator of cardiovascular reactivity. Given that a wide variety of AT1 receptor signalling pathways exists in neurones, the precise molecular mechanisms that underlie central cardiovascular actions of Ang II during emotional stress are yet to be determined. Growing evidence, however, indicates that reactive oxygen species, and in particular superoxide (·O2,), are important intracellular messengers of many actions of brain Ang II. In particular, studies employing microinjection of ·O2, scavengers directly into the rostral ventrolateral medulla (RVLM) and dorsomedial hypothalamus of rabbits have shown that the activation of AT1 receptor,·O2, signalling is required for full manifestation of the cardiovascular response to emotional stress. This role of ·O2, appears to be highly specific, because ·O2, scavengers in the RVLM do not alter the sympathoexcitatory response to baroreceptor unloading or sciatic nerve stimulation. The subcellular mechanisms for the stress-induced ·O2, production are likely to include the activation of NADPH oxidase and are essentially independent of nitric oxide. This review summarizes current knowledge of redox-sensitive signalling mechanisms in the brain that regulate cardiovascular effects of stress. Additionally, it presents initial evidence that ·O2, may be less important in the activation of central pressor pathways mediating cardiovascular arousal associated with appetitive events, such as food anticipation and feeding. [source]

Direct Evidence for Imidazoline (I1) Receptor Modulation of Ethanol Action on Norepinephrine-Containing Neurons in the Rostral Ventrolateral Medulla in Conscious Spontaneously Hypertensive Rats

Differential expression of catecholamine biosynthetic enzymes in the rat ventrolateral medulla

THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2001
Jacqueline K. Phillips
Abstract Adrenergic (C1) neurons located in the rostral ventrolateral medulla are considered a key component in the control of arterial blood pressure. Classically, C1 cells have been identified by their immunoreactivity for the catecholamine biosynthetic enzymes tyrosine hydroxylase (TH) and/or phenylethanolamine N-methyltransferase (PNMT). However, no studies have simultaneously demonstrated the expression of aromatic L-amino acid decarboxylase (AADC) and dopamine ,-hydroxylase (DBH) in these neurons. We examined the expression and colocalization of all four enzymes in the rat ventrolateral medulla using immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) analysis. Retrograde tracer injected into thoracic spinal segments T2,T4 was used to identify bulbospinal neurons. Using fluorescence and confocal microscopy, most cells of the C1 group were shown to be double or triple labeled with TH, DBH, and PNMT, whereas only 65,78% were immunoreactive for AADC. Cells that lacked detectable immunoreactivity for AADC were located in the rostral C1 region, and approximately 50% were spinally projecting. Some cells in this area lacked DBH immunoreactivity (6.5,8.3%) but were positive for TH and/or PNMT. Small numbers of cells were immunoreactive for only one of the four enzymes. Numerous fibres that were immunoreactive for DBH but not for TH or PNMT were noted in the rostral C1 region. Single-cell RT-PCR analysis conducted on spinally projecting C1 neurons indicated that only 76.5% of cells that contained mRNA for TH, DBH, and PNMT contained detectable message for AADC. These experiments suggest that a proportion of C1 cells may not express all of the enzymes necessary for adrenaline synthesis. J. Comp. Neurol. 432:20,34, 2001. © 2001 Wiley-Liss, Inc. [source]

Regulation of sympathetic tone and arterial pressure by rostral ventrolateral medulla after depletion of C1 cells in rat

THE JOURNAL OF PHYSIOLOGY, Issue 1 2000
Ann M. Schreihofer
1In this study we examined whether the rostral ventrolateral medulla (RVLM) maintains resting sympathetic vasomotor tone and activates sympathetic nerve activity (SNA) after the depletion of bulbospinal C1 adrenergic neurones. 2Bulbospinal C1 cells were destroyed (,84% loss) by bilateral microinjections (spinal segments T2 -T3) of an anti-dopamine-,-hydroxylase antibody conjugated to the ribosomal toxin saporin (anti-D,H-SAP). 3Extracellular recording and juxtacellular labelling of bulbospinal barosensitive neurones in the RVLM revealed that treatment with anti-D,H-SAP spared the lightly myelinated neurones with no tyrosine hydroxylase immunoreactivity. 4In rats treated with anti-D,H-SAP, inhibition of RVLM neurones by bilateral microinjection of muscimol eliminated splanchnic SNA and produced the same degree of hypotension as in control rats. 5Following treatment with anti-D,H-SAP the sympathoexcitatory (splanchnic nerve) and pressor responses to electrical stimulation of the RVLM were reduced. 6Treatment with anti-D,H-SAP also eliminated the majority of A5 noradrenergic neurones. However, rats with selective lesion of A5 cells by microinjection of 6-hydroxydopamine into the pons showed no deficits to stimulation of the RVLM. 7In summary, the loss of 84% of bulbospinal adrenergic neurones does not alter the ability of RVLM to maintain SNA and arterial pressure at rest in anaesthetized rats, but this loss reduces the sympathoexcitatory and pressor responses evoked by RVLM stimulation. The data suggest sympathoexcitatory roles for both the C1 cells and non-C1 cells of the RVLM and further suggest the C1 cells are critical for the full expression of sympathoexcitatory responses generated by the RVLM. [source]

Adrenomedullin in the rostral ventrolateral medulla inhibits baroreflex control of heart rate: a role for protein kinase A

BRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2006
Yong Xu
1The rostral ventrolateral medulla (RVLM) is an essential vasomotor center in the brainstem which participates in maintaining resting levels of arterial pressure and for regulating baroreflex activity. We have demonstrated that microinjections of adrenomedullin (ADM), a vasoactive neuropeptide, into the RVLM cause increased resting mean arterial pressure (MAP) and heart rate (HR). However, the effect of ADM on baroreflex function remains unclear. 2The purposes of the present study were to investigate the effect of ADM in the RVLM on the regulation of baroreflex activity and to identify the underlying mechanisms. Baroreflex curves were generated with intravenous injections of multiple doses of phenylephrine and nitroprusside. The upper and lower plateaus, reflex range, MAP at the midpoint of HR range (MAP50), and gain were evaluated before and after various microinjections were made into the RVLM of urethane-anesthetized rats. 3Microinjections of ADM decreased the upper plateau, reflex range, and gain, and increased MAP50, indicating that ADM in the RVLM impairs baroreflex function. 4ADM22,52, a putative ADM receptor antagonist, significantly increased the baroreflex gain and upper plateau, demonstrating that endogenous ADM tonically inhibits the baroreflex. Coinjections of ADM22,52 with ADM blocked the ADM-induced baroreflex responses. 5ADM's effect was abolished with H-89, a protein kinase A (PKA) inhibitor. 6Our results show that ADM in the RVLM exerts an inhibitory effect on baroreflex activity via an ADM receptor-mediated mechanism, and that activation of PKA is involved in this event. British Journal of Pharmacology (2006) 148, 70,77. doi:10.1038/sj.bjp.0706698 [source]

Orthostatic hypotension associated with dorsal medullary cavernous angioma

ACTA NEUROLOGICA SCANDINAVICA, Issue 1 2009
J. Idiaquez
Background,,, Orthostatic hypotension (OH) is a rare manifestation of medulla oblongata lesions that may be because of interruption of descending sympathoexcitatory axons. Aims,,, To illustrate the location of a medullary lesion that produced OH following resection in relationship to the location of putative sympathoexcitatory pathways. Method,,, A case with dorsal medullary cavernous angioma presenting with OH is described. The possible localization of lesion was compared with distribution of tyrosine hydroxylase (TH)-immunoreactive axons in a comparable section of the medulla of a control brain. Results,,, The patient had marked OH after partial removal of the cavernous angioma. Biopsy confirmed the diagnosis. The magnetic resonance imaging location of the lesion overlapped that of TH-immunoreactive axons of the medullary transtegmental tract. Conclusions,,, A restricted lesion of medullary lesion interrupting the catecholaminergic transtegmental tract arising from the sympathoexcitatory C1 neurons of the rostral ventrolateral medulla could result in severe OH. [source]

EFFECTS OF MELATONIN ON BLOOD PRESSURE IN STRESS-INDUCED HYPERTENSION IN RATS

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2008
Chun-Mei Xia
SUMMARY 1Melatonin, acting through its receptors, is involved in numerous physiological processes, including blood pressure (BP) regulation. In present study, the effect of melatonin inhibition on stress-induced hypertension was investigated. 2The hypertensive model consisted of male Sprague-Dawley rats subjected to electrical foot-shock combined with noise. Microinjection of melatonin (0.1 and 1.0 mmol/L) into the anterior hypothalamic area (AHA) produced a fall in BP in nomortensive rats and stress-induced hypertensive rats (SIHR). Luzindole (10 mmol/L), a competitive antagonist of melatonin MT1 and MT2 receptors, almost completely abolished the depressor effect of melatonin, the MT2 receptor-specific antagonist 4-phenyl-2-propionamidotetralin (10 mmol/L) partially blocked (by approximately 60%) the depressor effect of melatonin, whereas the MT3 receptor-selective antagonist prazosin (10 mmol/L) failed to antagonize the effects of melatonin. 3Brain microdialysis was performed in the AHA and the rostral ventrolateral medulla (RVLM). Melatonin and amino acids in the dialysate samples collected were detected by high-performance liquid chromatography combined with fluorescence detection. The results indicated that melatonin concentrations in the AHA were reduced in SIHR. Microinjection of melatonin into the AHA decreased glutamate release and increased GABA and taurine release in the RVLM, which were paralleled by a decrease in arterial pressure. 4The mRNA expression of MT2 in the AHA of SIHR was higher than that in normotensive control rats, whereas there was no significant difference in MT1 mRNA expressin between the two groups. 5The results of the present study suggest that both a decrease of melatonin and an increase in the MT2 receptor in the AHA are involved in the manifestation of stress-induced hypertension. Both MT1 and MT2 receptors participated in the antihypertensive effect of melatonin in the AHA. The antihypertensive effect of melatonin was related to the decreases in the excitatory amino acid glutamate and increases in the inhibitory amino acids taurine and GABA in the RVLM. [source]

Inhibitory Effects Of Angiotensin Ii On Barosensitive Rostral Ventrolateral Medulla Neurons Of The Rat

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2001
Delphine Bertram
SUMMARY 1. The brain renin,angiotensin system can influence arterial baroreceptor reflex control of blood pressure (BP) through both direct and indirect effects on sympathetic premotor neurons of the rostral ventrolateral medulla (RVLM). The present study examined the direct effect of angiotensin (Ang) II applied by microiontophoresis on the ongoing activity of single RVLM neurons. 2. In 26 urethane-anaesthetized Wistar rats, recordings of single unit activities of barosensitive RVLM neurons were made from one barrel of a six-barrel micropipette assembly. The other five barrels were filled with either L -glutamate, AngII, valsartan (an AT1 receptor antagonist), PD 123177 (an AT2 receptor antagonist) and saline. All drugs were applied by microiontophoresis. 3. Mean BP was 83 ± 3 mmHg. Application of AngII inhibited the ongoing activity of RVLM neurons, identified as barosensitive because their activity was inhibited by a phenylephrine- induced increase in BP, from 12.6 ± 1.5 to 5.4 ± 1.1 Hz (n = 24; P < 0.001). Angiotensin II also inhibited the glutamate-evoked excitation of barosensitive RVLM neurons from 15 ± 3 to 5.8 ± 2.0 Hz (n = 6; P < 0.001). Valsartan significantly increased neuronal activity from 9.5 ± 2.3 to 13.5 ± 3.2 Hz (n = 7, P < 0.01), whereas PD 123177 significantly decreased neuronal activity from 13.5 ± 3.5 to 9.9 ± 2.8 Hz (n = 13; P < 0.01). 4. The results suggest that AngII exerts a tonic inhibitory effect on barosensitive RVLM neurons, which is presumably mediated through AT1 receptor stimulation. [source]

Role Of Nitric Oxide On Pressor Mechanisms Within The Dorsomedial And Rostral Ventrolateral Medulla In Anaesthetized Cats

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2001
Shu-Ying Chen
SUMMARY 1. The role of nitric oxide (NO) in central cardiovascular regulation and the correlation between NO and glutamate-induced mechanisms is not clear. Microinjection of glutamate (3 nmol/ 30 nL) into dorsomedial medulla (DM) and rostral ventrolateral medulla (RVLM) increased arterial blood pressure (BP) and sympathetic vertebral nerve activity (VNA). Thus, in the present study, we examined the modulation by NO of glutamate-induced pressor responses in the DM and RVLM of cats. 2. Histochemical methods using nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) as a marker to stain neurons containing NO synthase (NOS), showed positive findings of NOS in both the DM and RVLM. 3. Microinjection of NG -nitro- L -arginine methyl ester (L -NAME), a NOS inhibitor, into the DM or RVLM did not alter resting BP and VNA, but it did cause a dose-dependent attenuation of glutamate-induced pressor responses. Interestingly, the increase in NO levels that resulted from pretreatment with L -arginine (L -Arg) or sodium nitroprusside (SNP) did not alter resting BP and VNA, but still inhibited glutamate-induced pressor responses in the DM and RVLM in a dose-dependent manner. 4. We also examined whether NO modulated the pressor responses induced by activation of different excitatory amino acid receptors. N -Methyl- D -aspartate (NMDA) and , -amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) were used. Consistent with the results from the initial glutamate studies, we observed that not only L -NAME, but also L -Arg and SNP attenuated pressor responses induced by NMDA and AMPA. No difference was found between the effects of NO on NMDA- and AMPA-induced pressor responses. 5. To investigate the possibility of a loss of agonist selectivity, the effects of D -2-amino-5-phosphonovalerate (D -AP5) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) on AMPA and NMDA responses in the DM were examined. The results showed that CNQX did not alter NMDA-induced pressor responses, while D -AP5 failed to alter AMPA-induced responses. 6. Our results suggest that activation of the glutamate-induced pressor mechanism is regulated by changes in NO levels in the DM and RVLM. This implies that NO may play a permissive role to allow operation of the glutamate-activation mechanism. [source]

Proceedings of the Australian Physiological and Pharmacological Society Symposium: The Hypothalamus HYPOTHALAMIC PARAVENTRICULAR NUCLEUS AND CARDIOVASCULAR REGULATION

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2001
Emilio BadoerArticle first published online: 10 DEC 200
SUMMARY 1. The hypothalamic paraventricular nucleus (PVN) is an important integrative site within the brain composed of magnocellular and parvocellular neurons. It is known to influence sympathetic nerve activity. 2. The parvocellular PVN contains neurons that project to the intermediolateral cell column of the thoraco,lumbar spinal cord (IML). This defines the PVN as an autonomic ,premotor nucleus', one of only five present within the brain. 3. Another projection arising from the PVN is a prominent innervation of the pressor region of the rostral ventrolateral medulla (RVLM), also a premotor nucleus. The distribution of the PVN neurons projecting to the RVLM is similar to that of the PVN neurons that project to the IML. 4. It has been found that up to 30% of spinally projecting neurons in the PVN also send collaterals to the RVLM. Thus, there are neurons in the PVN that can: (i) directly influence sympathetic nerve activity (via PVN,IML connections); (ii) indirectly influence sympathetic nerve activity (via PVN,RVLM connections); and (iii) both directly and indirectly influence sympathetic nerve activity (via neurons with collaterals to the IML and RVLM). 5. In the rat, results of studies using the protein Fos to identify activated neurons in the brain suggest that neurons in the PVN with projections to the IML or RVLM may be activated by decreases in blood volume. 6. In conclusion, the PVN can influence sympathetic nerve activity. Within the PVN are neurons with anatomical connections that enable them to affect sympathetic nerve activity either directly, indirectly or via both mechanisms (via collaterals). Studies that have examined the role of specific subgroups within the PVN suggest that PVN neurons with connections to the IML or to the RVLM may play a role in the reflex changes in sympathetic nerve activity that are involved in blood volume regulation. [source]

Area Postrema And Sympathetic Nervous System Effects Of Vasopressin And Angiotensin II

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2000
Eileen M Hasser
SUMMARY 1. Precise control over the cardiovascular system requires the integration of both neural and humoral signals related to blood volume and blood pressure. Humoral signals interact with neural systems, modulating their control over the efferent mechanisms that ultimately determine the level of pressure and volume. 2. Peptide hormones such as angiotensin (Ang)II and arginine vasopressin (AVP) act through circumventricular organs (CVO) to influence cardiovascular regulation. 3. The area postrema (AP), a CVO in the brainstem, mediates at least some of the central actions of these peptides. Vasopressin appears to act in the AP to cause sympathoinhibition and a shift in baroreflex control of the sympathetic nervous system (SNS) to lower pressures. These effects of AVP and the AP appear to be mediated by ,2 -adrenoceptor and glutamatergic mechanisms in the nucleus tractus solitarius. 4. In contrast to AVP AngII has effects in the AP to blunt baroreflex control of heart rate and cause sympathoexcitation. The effects of chronic AngII to increase activity of the SNS may be due to AP-dependent activation of neurons in the rostral ventrolateral medulla. [source]