Rostral Ventrolateral Medulla Of Rats Research Articles

P-126 - Cardiovascular effects of neuropeptides injected into the rat rostral ventrolateral medulla.

P-126 - Cardiovascular effects of neuropeptides injected into the rat rostral ventrolateral medulla.

Stereoselective effects of central α2-adrenergic agonist medetomidine on in vivo catechol activity in the rat rostral ventrolateral medulla (RVLM)

The stereoselective central effects of a novel, highly potent and selective α 2-agonist medetomidine on adrenergic neuronal activity, reflected by changes in catechol oxidation current, in the rostral ventrolateral medulla of the halothane-anesthetized rat were examined using in vivo differential normal pulse voltammetry. Dexmedetomidine, the active isomer, significantly decreased catechol oxidation current to 33.4±4.5% of baseline when given centrally (1 μg, i.c.v.) and to 10.3±3.9% of baseline when given systemically (50 μg/kg, i.v.). Dexmedetomidine also significantly reduced mean arterial blood pressure by 19.9% following central administration but significantly increased mean arterial blood pressure by 59.9% following systemic administration. Levomedetomidine, the inactive isomer, had no effect on catechol oxidation current or blood pressure. The depressant effects of dexmedetomidine on catechol oxidation current were reversed by the selective α 2-adrenoceptor antagonist atipamezole (2 μg, i.c.v. or 200 μg/kg, i.v.). The results of the present study demonstrate, to our knowledge, for the first time the central stereoselective effects of medetomidine and antagonism by atipamezole on rostral ventrolateral medulla activity in the anesthetized rat.

Characterization of coronary vasoconstriction produced by rostral ventrolateral medulla stimulation in rats.

Previous studies have demonstrated that coronary vasoconstriction can be produced by activation of specific central nervous system sites in the cat. The present study was undertaken 1) to develop a rat model for studying central influences on coronary circulation and 2) to utilize this model for characterization of the changes in coronary blood flow (CBF) produced by stimulation of rostral ventrolateral medulla (RVLM). Electrical stimulation of right RVLM in chloralose-anesthetized rats with bilateral vagotomy produced a transient decrease in CBF followed by an increase in CBF concomitant with a decrease in hindquarter blood flow, a pressor response, and tachycardia. After atenolol the tachycardia and increase in CBF were abolished, whereas the decrease in CBF was enhanced and prolonged. Phentolamine (1 mg/kg iv) or removal of the stellate ganglia inhibited the decrease in CBF but did not totally abolish the increase in coronary vascular resistance. Inhibition of nitric oxide synthesis with N-nitro-L-arginine (10 microM/kg iv) enhanced the decrease in CBF produced by stimulation in RVLM. These results indicate that, in rat model, the centrally induced decrease in CBF is 1) mediated by cardiac sympathetic innervation but only partially through alpha-adrenoceptors and 2) enhanced by removal of the inhibitory effect of the endothelium.

Intracellular analysis in vivo of different barosensitive bulbospinal neurons in the rat rostral ventrolateral medulla

Neurons located in the rostral ventrolateral medulla (RVLM) with projections to the intermediolateral column (IML) in the spinal cord were electrophysiologically characterized and anatomically identified using an intracellular recording technique in vivo. A group of spontaneously active neurons was antidromically activated by electrical stimulation of the IML in the thoracic spinal cord (T2-T3 level). The axonal conduction velocities ranged from 1.5 m/sec to 11.0 m/sec; mean value, 5.5 +/- 2.6 m/sec (+/- SD). The firing pattern and changes in membrane potential in relation to the cardiac cycle were investigated in these bulbospinal neurons. A first group discharged action potentials with higher frequency at the end of the diastolic/beginning of the systolic period. The average of the neuronal membrane potentials demonstrated depolarizing potentials at the end of the diastolic/beginning of the systolic period. These depolarizing potentials increased in magnitude when the neurons were hyperpolarized. Therefore, they were characterized as EPSPs. The baroreceptor reflex activation produced by the increase in systemic arterial pressure following intravenous injection of phenylephrine elicited hyperpolarization, a decrease in the rate of discharge, and an increase in the membrane input resistance, suggesting that a disfacilitatory effect was produced by the activation of baroreceptor inputs on these bulbospinal neurons. Conversely, the inactivation of the baroreceptor reflex by intravenous injection of sodium nitroprusside produced depolarization and an increase in the firing rate. These neurons were characterized as baroreceptor-sensitive type I neurons. A second group of bulbospinal neuron in the RVLM was differentiated from the first group because it demonstrated a decrease in the frequency of discharge at the end of the diastolic/beginning of the systolic period. The average of the membrane potentials showed hyperpolarizing potentials that decreased in magnitude when the neuron was hyperpolarized. These hyperpolarizing potentials occurred at the end of the diastolic/beginning of the systolic period and were reversed in polarity after intracellular injections of chloride ions for several minutes. Therefore, these potentials were characterized as chloride-dependent IPSPs locked to the cardiac cycle. In some of these neurons, the electrical stimulation of the IML produced, in addition to the antidromic action potential, a monosynaptic EPSP with a shorter latency. Based on these unique characteristics, these neurons were defined as barosensitive type II neurons. During constant baroreceptor inactivation achieved by the hypotension produced by intravenous infusions of sodium nitroprusside, the pattern of discharge of barosensitive type II neurons became very regular, and the IPSPs locked to the cardiac cycle were absent.(ABSTRACT TRUNCATED AT 400 WORDS)

Modulation of Norepinephrine Release in Blood Vessels

Summary: Various imidazoline and guanidine derivatives with agonistic or antagonistic properties at α2-adrenoceptors may modulate norepinephrine release not only via classic α2-autoreceptors but also via presynaptic imidazoline receptors. This possibility was examined in rabbit pulmonary artery and aorta preincubated with [3H]norepinephrine (NE) and superfused with a physiological salt solution. The release of [3H]NE from the sympathetic nerves contained in the preparations was stimulated by electrical impulses (2 Hz, unless stated otherwise). α2-Adrenoceptor-blocking imidazolines such as phentolamine, tolazoline, idazoxan, and 4-chloro-2-(2-imidazoline-2-ylamino)-isoindoline (BDF 6143) increased the electrically evoked [3H]NE release. Their concentration-response curves were bell-shaped, and the maximum increase obtainable was less than that obtained with rauwolscine, a nonimidazoline α2-adrenoceptor antagonist. When the frequency of stimulation was decreased from 2 to 0.66 Hz (leading to a decreased concentration of NE in the biophase of the α2-autoreceptors and therefore a decreased degree of autoreceptor activation), BDF 6143 no longer facilitated but instead concentration-dependently inhibited [3H]NE release. An inhibition of release without any facilitatory component could also be observed at 2 Hz with all imidazoline derivatives mentioned above when the presynaptic α2-adrenoceptors had been blocked by rauwolscine and/or preexposure to the irreversible α-adrenoceptor antagonist phenoxybenzamine. Clonidine and moxonidine, two imidazolines with α2-adrenoceptor agonistic properties, and cirazoline, an imidazoline devoid of intrinsic activity at α2-adrenoceptors, inhibited [3H]NE release. Rauwolscine apparently was antagonistic not only at presynaptic α2-adrenoceptors but also at presynaptic imidazoline receptors because it antagonized the inhibitory response to BDF 6143 at 0.66 Hz. The pA2 values of rauwolscine for α2-adrenoceptor antagonism in various tissues of several species (reported in the literature) were, as a rule, in the range of 8.0. In the rabbit pulmonary artery and aorta, pA2 values of rauwolscine in this range could be found only for the antagonism against the moxonidine-induced inhibition of [3H]NE release, whereas the pA2 values against clonidine and other putative imidazole receptor agonists were between 6.37 and 6.77. Taken together, the present data suggest that in addition to the classic α2-adrenoceptors, imidazoline receptors are involved in modulation of NE release in the rabbit pulmonary artery and aorta. Comparison of the potencies of all putative imidazoline receptor-ligands investigated in these blood vessels with their potencies in other tissues (including those in the rostral ventrolateral medulla of the brainstem involved in the hypotensive effect of clonidine and moxonidine) revealed that the imidazoline sites are heterogeneous. In the rabbit pulmonary artery and aorta, moxonidine activates predominantly α2-adrenoceptors (but not the coexisting presynaptic imidazoline receptors subtype), whereas it possesses particularly high affinity for the imidazoline receptors in the rat rostral ventrolateral medulla. Thus. moxonidine may be particularly selective for the imidazoline receptor of the brainstem.

Effect of clonidine on catechol metabolism in the rostral ventrolateral medulla: an in vivo electrochemical study

The dose-dependent reduction in catechol metabolism induced by an imidazoline with α 2-adrenoceptor agonist specificity, clonidine, was assessed ( ED 50 = 7 μg · kg −1 i.v.) with in vivo voltammetry in the rostral ventrolateral medulla of rats kept under halothane anesthesia and strictly controlled circulatory and ventilatory conditions. This reduction in catechol metabolism was observed in intact as well as in barodeafferented rats.

NMDA antagonists attenuate hypertension induced by carotid clamping in the rostral ventrolateral medulla of rats

The purpose of these experiments were to study the interactions of N-methyl-D-aspartate (NMDA) with baroreceptor reflexes induced by transient carotid clamping. Adult male Sprague-Dawley rats were anesthetized with urethane. Bilateral common carotid artery occlusion resulted in a reversible and reproducible hypertension in the vagotomized animals. This hypertensive reaction was blocked by intraventricular injection of NMDA antagonists, such as 2-amino-7-phosphono-heptaneoate (AP-7) and phencyclidine (PCP). We also found that blood pressure-sensitive neurons of the rostral ventrolateral medulla (RVLM) could be classified into two groups, on the basis of their responses to norepinephrine given intravenously. Using pressure microejection and single unit recording, we observed that clamping of the common carotids resulted in excitation of type I neurons. This evoked excitation, similar to that induced by NMDA, was blocked by locally applied AP-7. However, the carotid occlusion-induced responses of type II neurons were not blocked by AP-7. In conclusion, the present data suggest that NMDA receptors are involved in hypertensive responses during carotid occlusion, perhaps involving a site in the rostral ventrolateral medulla.

Antinociceptive and behavioral effects of low dose kainic acid injections into the pag of the rat

Nitric oxide (NO) within the brain is known to have an important influence on sympathetic nerve activity (SNA). NO is found in the paraventricular nucleus (PVN), caudal ventrolateral medulla (CVLM) and the nucleus tractus solitarius (NTS), regions that project to the rostral ventrolateral medulla (RVLM), an area that is critical in the regulation of SNA. The aim of the present study was to determine whether neurons in the PVN, NTS and CVLM that project to the RVLM contain the neuronal isoform of nitric oxide synthase (nNOS) and are, therefore, capable of producing NO. Under pentobarbitone general anaesthesia, the retrogradely-transported tracer, rhodamine-tagged microspheres, were microinjected into the RVLM of rats (n = 6). Two weeks later, the animals were re-anaesthetised, perfused with para-formaldehyde and the brains were removed. Hypothalamic and medullary sections were processed for nNOS immunohistochemistry and the RVLM-projecting neurons were identified using fluorescence microscopy. We found nNOS-containing neurons were present throughout the PVN, CVLM and NTS and that these were intermingled with neurons that projected to the RVLM. Of the neurons in the PVN and CVLM that projected to the RVLM, approximately 12 ± 1% and 8 ± 3%, respectively, contained nNOS. In the NTS only 1 ± 1% of the neurons were double-labeled. This study highlights anatomical pathways emanating from the PVN and CVLM, in particular, which may contribute to the effects on SNA elicited by NO within the brain.

Pharmacological and functional evidence for extracellular 3,4-dihydroxyphenylacetic acid as an index of metabolic activity of the adrenergic neurons: An in vivo voltammetry study in the rat rostral ventrolateral medulla

Catecholamine metabolism was studied in vivo in the Cl adrenergic area of the rostral ventrolateral medulla oblongata in rats, using differential normal pulse voltammetry coupled with an activated carbon fiber microelectrode. Pharmacological evidence indicates that 3,4-dihydroxyphenylacetic acid, the major dopamine metabolite, is responsible for the electrochemical signal appearance in the C1 group, and that it reflects the Catecholamine synthesis rate, as previously reported in the locus coeruleus. Indeed, 3,4-dihydroxyphenylacetic acid was estimated to be formed from 77% of the intracellular dopamine, since its synthesis was increased by only 23%, after blockade of the dopamine-β-hydroxylase activity. Neuronal activation by retrograde electrical stimulation increased the electrochemical signal, as well as hemorrhage and hypotension, suggesting that the level of extracellular 3,4-dihydroxyphenylacetic acid is a good biochemical index of the C1 adrenergic cellular activity in baseline conditions and during cellular activation.

Ultrastructural localization of choline acetyltransferase in the rat rostral ventrolateral medulla: evidence for major synaptic relations with non-catecholaminergic neurons

Pharmacological and biochemical studies suggest that interactions between cholinergic and catecholaminergic neurons, particularly those of the C1 adrenergic cell group, in the rostral ventrolateral medulla (RVL) may be important in cardiovascular control. Ultrastructural localization of choline acetyltransferase (ChAT), the biosynthetic enzyme for acetylcholine, and its relation to neurons exhibiting immunoreactivity for catecholamine- (tyrosine hydroxylase; TH) or adrenaline (phenylethanolamine- N-methyltransferase; PNMT) -synthesizing enzymes were examined in the RVL using dual immunoautoradiographic and peroxidase anti-peroxidase (PAP) labeling methods. By light microscopy, the ChAT-immunoreactive neurons were located both dorsally (i.e. the nucleus ambiguus) and ventromedially to those labeled with TH or PNMT (TH/PNMT). A few ChAT-labeled processes were dispersed among TH/PNMT-containing neurons with the majority of overlap immediately ventral to the nucleus ambiguus. By electron microscopy, ChAT-immunoreactivity (ChAT-I) was detected in neuronal perikarya, dendrites, axons and axon terminals and in the vascular endothelial cells of certain blood vessels. The ChAT-labeled perikarya in the ventromedial RVL were medium-sized (15–20 μm), elongated, contained abundant cytoplasm and had slightly indented nuclei. Synaptic junctions on ChAT-immunoreactive perikarya and dendrites were primarily symmetric with 64% (45 out of 70) of the presynaptic terminals unlabeled. The remaining terminals were immunoreactive for ChAT (30%) or TH/PNMT (6%). Terminals with ChAT-I were large (0.8–2.0 μm) and contained numerous small clear vesicles and 1–2 dense core vesicles. Seventy-seven percent (112 out of 145) of the ChAT-labeled terminals formed symmetric synapses with unlabeled perikarya and dendrites, whereas only 8% were with TH/PNMT-labeled perikarya and dendrites, and 15% were with ChAT-immunoreactive perikarya and dendrites. We conclude (1) that cholinergic neurons in the RVL principally terminate on and receive input from non-catecholaminergic neurons, and (2) that the reported sympathetic activation following application of cholinergic agents to the RVL may be mediated by cholinergic inhibition of local inhibitory interneurons. The observed synapses between ChAT and TH/PNMT-containing neurons suggests that cholinergic and adrenergic neurons additionally may exert a minor reciprocal control on each other and thus may modulate their response to the more abundant input from afferents containing other transmitters.

Cardiovascular responses and changes in neural activity in the rostral ventrolateral medulla elicited by electrical stimulation of the amygdala of the rat

Electrical stimulation of the central nucleus of the amygdala (ACe) in anesthetized animals produces a decrease in arterial pressure (AP) as a result of an overall decrease in peripheral resistance. As the cardiovascular neurons that presumably mediate these changes are located in the rostral ventrolateral medulla (RVLM) [11], we recorded spontaneous activity from 89 histologically verified units in the RVLM of urethan-anesthetized rats. Twenty-two of these units were classified as cardiovascular neurons because their spontaneous activity was inhibited by baroreceptor stimulation (2–4 μg phenylephrine i.v.) and displayed a cardiac cycle-related rhythmicity. Single or twin pulses (0.5 ms, 180 ± 55 μA) delivered once per second to arterial depressor sites in the ipsilateral ACe inhibited the activity of 18 of these neurons and excited 4. In 27 additional barosensitive neurons that lacked cardiac cycle rythmicity, a similar distribution of effects was obtained by electrical stimulation of the ACe: 13 inhibited, 5 excited, 9 not affected. Finally, 40 non-barosensitive units were found; stimulation of the ACe inhibited the activity of 16, excited 12 and had not effect in 12. These results are interpreted to indicate that the differential effects of ACe stimulation on different vascular beds are mediated probably by differential influences on cardiovascular neurons in the RVLM, and that functions other than respiratory and cardiovascular control are represented in the RVLM.

Involvement of central alpha- and beta-adrenoceptors in the pressor response to electrical stimulation of the rostral ventrolateral medulla in rats.

1. Electrical stimulation of the C1 area of the rostral ventrolateral medulla in rats elicits an increase in mean arterial pressure (MAP). 2. This increase in MAP is attenuated by intra-hypothalamic and intracisternal administration of the non-selective beta-adrenoceptor antagonist (+/-)-propranolol and the beta 2-selective antagonist ICI 118551. 3. The selective beta 1-antagonist atenolol and (+)-propranolol, which is inactive on beta-adrenoceptors, did not alter the increase in MAP produced by stimulation of the C1 area. 4. The alpha 2-adrenoceptor antagonist idazoxan enhanced the effects of C1 stimulation on MAP when administered either into the posterior hypothalamus or intracisternally. 5. The results indicate that beta 2- and alpha 2-receptors both have a role in the mediation of the rise in MAP during stimulation of the C1 area and that the receptors involved are located both within the hypothalamus and the spinal cord.

Rostral ventrolateral medullary neurons with intrinsic pacemaker properties are not catecholaminergic

Neurons of the rat rostral ventrolateral medulla with intrinsic pacemaker properties and immediately adjacent silent neurons were recorded in tissue slices, labeled intracellularly with the fluorescent dye Lucifer yellow, and the tissue was subsequently processed for the immunocytochemical detection of the catecholamine-synthesizing enzyme tyrosine-hydroxylase. Forty-five percent (9/20) of the silent neurons were tyrosine hydroxylase-immunoreactive, but none of the pacemaker cells were (0/15). We conclude that the ventrolateral reticular neurons with intrinsic pacemaker properties are not the C 1 adrenergic cells.

Hypotensive effects of lesions of the rostral ventrolateral medulla in rats are anesthetic-dependent

These studies were designed to determine if the hypotensive effects of bilateral electrolytic lesions of the rostral ventrolateral medulla are dependent on the type of anesthetic agent used. The lesions caused an immediate fall in mean arterial pressure (MAP) in rats anesthetized with urethane, α-chloralose or sodium pentobarbital. At 30 min after placement of the lesions, severe hypotension (MAP = 54 ± 5 mm Hg) persisted in the rats anesthetized with urethane. However, 30 min after placement of the lesions, the MAP of rats anesthetized with α-chloralose or sodium pentobarbital was 87 ± 9 mm Hg and 99 ± 10 mm Hg, respectively. Subsequent transection of the cervical spinal cord produced a much greater decrease in MAP in rats anesthetized with α-chloralose and sodium pentobarbital as compared to rats anesthetized with urethane. Heart rate was significantly lower after placement of the lesions in all 3 groups. We conclude that the magnitude of the hypotensive effect caused by placement of lesions in the rostral ventrolateral medulla is anesthetic-dependent and that the rostral ventrolateral medulla is not the only area of the central nervous system capable of maintaining vasomotor tone.

Reticulospinal vasomotor neurons of the rat rostral ventrolateral medulla: relationship to sympathetic nerve activity and the C1 adrenergic cell group

Neurons projecting from the rostral ventrolateral medulla (RVL) to the spinal cord were antidromically identified in rats anesthetized with urethane, paralyzed, and ventilated. The sites of lowest antidromic threshold were concentrated in the intermediolateral nucleus (IML). Their axonal conduction velocities were distributed bimodally, with the mean of the rapidly conducting fibers (greater than 1 m/sec) being 3.1 +/- 0.1 m/sec (n = 105), and of the slower axons being 0.8 +/- 0.03 m/sec (n = 25). Single-shock electrical stimulation of RVL elicited 2 bursts of excitation in splanchnic sympathetic nerve activity (SNA), which resulted from activation of 2 descending pathways with conduction velocities comparable to those of antidromically excited RVL-spinal neurons. The probability of discharge of RVL-spinal cells was synchronized both with the cardiac-related bursts in SNA with functional baroreceptor reflexes and with the free-running 2-6 Hz bursts in SNA following baroreceptor afferent denervation. On the average, their spontaneous discharges occurred 67 +/- 2 msec (n = 31) prior to the peak of the spontaneous bursts in splanchnic SNA. This time corresponded to the latency to the peak of the early excitatory potential in splanchnic SNA following electrical stimulation of RVL. Baroreceptor reflex activation inhibited RVL-spinal neurons. The recording sites of RVL-spinal vasomotor neurons were consistently located within 100 micron of cell bodies (C1 neurons) immunoreactive for the adrenaline-synthesizing enzyme phenylethanolamine N-methyltransferase (PNMT). Ultrastructural analysis of the lateral funiculus of the cervical and thoracic spinal cord demonstrated PNMT immunoreactivity within myelinated (0.6-2.1 micron diameter) and unmyelinated (0.1-0.8 micron diameter) axons. Estimated conduction velocities of these fibers were comparable to the antidromic conduction velocities of the rapidly and slowly conducting populations of RVL-spinal vasomotor neurons. We conclude that in rat, the discharge of RVL-spinal vasomotor neurons strongly influences SNA: the baroreceptor-mediated inhibition of these neurons is reflected in the cardiac locking of SNA, while, in the absence of baroreceptor input, the synchronous discharge of RVL-spinal neurons maintains a free-running 2-6 Hz bursting pattern in SNA. RVL-spinal neurons are located within, and may be elements of, the C1 adrenergic cell group, and they provide a sympathoexcitatory drive to neurons in the IML over rapidly and slowly conducting pathways that correspond to myelinated and unmyelinated spinal axons containing PNMT.

Reticulospinal pacemaker neurons of the rat rostral ventrolateral medulla with putative sympathoexcitatory function: an intracellular study in vitro

Extra- and intracellular recordings of tonically active neurons were obtained in slices of the rat rostral ventrolateral medulla maintained at 31°C. The predominant type consisted of cells with a regular non-bursting discharge rate of 9 ± 0.3 spikes/s (mean ± S.E.M., n = 84). Intracellular recordings revealed that these neurons ( n = 43) exhibited typical pacemaker potentials reset after a single spike, and an input resistance of 138 ± 10 MΩ (n = 21) . No excitatory postsynaptic potentials were detected even during hyperpolarization (5–10 mV) which invariably resulted in silencing the cells ( n = 28). Eighteen cells were injected intracellularly with Lucifer yellow, and the tissue was subsequently processed for the immunohistochemical detection of the adrenergic marker phenylethanolamine N-methyltransferase (PNMT). None of the 12 dye-marked cells recovered exhibited any PNMT-like immunoreactivity, but all were surrounded by numerous adrenergic neurons. In 7 rats subjected to intraspinal injections (T 3) of rhodamine-tagged microbeads. 4 out of 9 pacemaker cells marked intracellularly with Lucifer yellow were found labeled with the retrograde marker. It is concluded that the rostral ventrolateral medulla contains non-adrenergic reticulospinal cells with intrinsic pacemaker properties. These neurons probably represent a group of sympathoexcitatory cells on which the basal sympathetic tone depends.

Phenylethanolamine N-methyltransferase-containing neurons in the rostral ventrolateral medulla of the rat. I. Normal ultrastructure

The electron microscopic localization of the adrenaline-synthesizing enzyme, phenylethanolamine N-methyltransferase (PNMT) was examined in the rostral ventrolateral medulla (RVL) of adult rats. The brains were fixed by perfusion with 3.75% acrolein and 2.0% paraformaldehyde in phosphate buffer. Coronal Vibratome sections through the RVL were immunocytochemically labeled using a rabbit polyclonal antiserum to PNMT and the peroxidase-antiperoxidase method. A semi-quantitative ultrastructural analysis revealed that the perikarya constituted 9% of the total immunoreactive profiles observed in the RVL. The labeled somata were large (18–24 μm) and were characterized by an indented nucleus and abundant cytoplasm with numerous mitochondria. An average of136.8 ± 11.6 mitochondria were present per 100 μm 2 cytoplasm, which is 38% greater than the numbers found for PNMT-immunoreactive neurons in the nucleus of the solitary tract. Moreover, the labeled somata were often found in direct apposition to the basal lamina of small capillaries and neighboring astrocytic processes. The remaining labeled profiles were neuronal processes of which 72% were dendrites. Both the PNMT-labeled somata and dendrites received primarily symmetric contacts from unlabeled axon terminals. Only a few axons and terminals containing immunoreactivity for PNMT were observed. The axons were both unmyelinated and myelinated. The PNMT-immunoreactive terminals were characterized by a mixed population of vesicles and by the formation of synaptic junctions with both unlabeled dendrites and PNMT-labeled perikarya and dendrites. The ultrastructural morphology and proximity to blood vessels and glia suggest a high metabolic activity and possibly a chemosensory function of PNMT neurons in the RVL. The existence of myelinated and unmyelinated axons could imply that PNMT-containing neurons have different conduction velocities in efferent pathways to the spinal cord or other brain regions. Furthermore, the multiple types of synaptic interactions between labeled and unlabeled axons and dendrites support the concept that adrenergic neurons modulate and are modulated by neurons containing the same or other putative transmitters in the RVL.

Electrophysiological study of cardiovascular neurons in the rostral ventrolateral medulla in rats.

In urethane-anesthetized rats, electrophysiological recordings of spontaneously active neurons in the vasopressor area of the rostral ventrolateral medulla were analyzed for participation in cardiovascular regulation. A total of 138 units were found which were inhibited by transient increases in mean arterial pressure elicited by intravenous injection of norepinephrine, aortic occlusion, or electrical stimulation of the hypothalamus, with 100% inhibition occurring at 148 mm Hg. Histograms of postsystolic activity showed that these units had pulse-synchronous rhythms which grew more prominent as arterial pressure increased. Furthermore, electrical stimulation of the superior laryngeal nerve, which elicited a vasodepressor response, strongly inhibited these units. Thus, these neurons were termed negatively correlated cardiovascular units. At least half of these cells project to or through the thoracic spinal cord. In addition, arterial pressure sensitivity is conveyed through carotid sinus and aortic arch afferents. Approximately half of the cardiovascular units are also excited by hypothalamic stimulation. Finally, analysis of neighboring cells showed that it is possible to distinguish between cardiovascular and respiratory units. These data are consistent with the concept of a medullary center which supports tonic sympathetic vasomotor tone and which mediates baroreceptor reflexes, as well as vascular responses of the defense reaction.

Release of a humoral vasodilator substance during neurogenic vasodilatation.

ARTICLESRelease of a humoral vasodilator substance during neurogenic vasodilatationDR Ballard, FM Abboud, and HE MayerDR Ballard, FM Abboud, and HE MayerPublished Online:01 Nov 1970https://doi.org/10.1152/ajplegacy.1970.219.5.1451MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByThe pressor effect of angiotensin-(1-7) in the rat rostral ventrolateral medulla involves multiple peripheral mechanismsClinics, Vol. 68, No. 2Role of nitrosyl factors in the hindlimb vasodilation elicited by baroreceptor afferent nerve stimulationOlga S. Possas, Alan Kim Johnson, and Stephen J. Lewis1 March 2006 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 290, No. 3Hypotensive effect of ANG II and ANG-(1–7) at the caudal ventrolateral medulla involves different mechanismsA. C. Alzamora, R. A. S. Santos, and M. J. Campagnole-Santos1 November 2002 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 283, No. 5Vasodilatation of muscle microvessels induced by somatic afferent stimulation is mediated by calcitonin gene-related peptide release in the ratNeuroscience Letters, Vol. 333, No. 2Inhibition of sympathetic cholinergic vasodilatation by a selective NPY Y2 receptor agonist in the gracilis muscle of anaesthetised dogsJournal of the Autonomic Nervous System, Vol. 68, No. 1-2Neurogenic cutaneous vasodilation in the cat forepawJournal of the Autonomic Nervous System, Vol. 37, No. 1Inhibition of carrageenan induced inflammation in the rat knee joint by substance P antagonist.Annals of the Rheumatic Diseases, Vol. 48, No. 11In search of mediators of skin vasodilation induced by transcutaneous nerve stimulation: III. Increase in plasma VIP in normal subjects and in Raynaud's DiseaseGeneral Pharmacology: The Vascular System, Vol. 15, No. 2In search of mediators of skin vasodilation induced by transcutaneous nerve stimulation: IV. In vitro bioassay of the vasoinhibitory activity of sera from patients suffering from peripheral ischaemiaGeneral Pharmacology: The Vascular System, Vol. 15, No. 2Interaction of Cardiovascular Reflexes in Circulatory Control1 January 2011Cardiovascular Adjustments to Thermal Stress1 January 2011In search of mediators of skin vasodilation induced by transcutaneous nerve stimulation: I. Failure to block the response by antagonists of endogenous vasodilatorsGeneral Pharmacology: The Vascular System, Vol. 14, No. 6Dopamine as a postganglionic autonomic neurotransmitterNeuroscience, Vol. 7, No. 1Adenosine triphosphate-evoked vascular changes in human skin: Mechanism of actionEuropean Journal of Pharmacology, Vol. 76, No. 4Cholinergic and Purinergic Regulation of Blood Vessels1 January 2011EVIDENCE FOR DOPAMINERGIC VASODILATOR INNERVATION OF THE CANINE PAW PAD19 July 2012 | British Journal of Pharmacology, Vol. 67, No. 3Substance P as neurogenic mediator of antidromic vasodilation and neurogenic plasma extravasationNaunyn-Schmiedeberg's Archives of Pharmacology, Vol. 310, No. 2Components of the hemodynamic response to elevated cerebrospinal fluid pressureAmerican Heart Journal, Vol. 95, No. 1Neurogenic vasodilatationGeneral Pharmacology: The Vascular System, Vol. 9, No. 4AUTONOMIC NEUROEFFECTOR JUNCTIONS—REFLEX VASODILATATION OF THE SKINJournal of Investigative Dermatology, Vol. 69, No. 1REFLEX CONTROL OF THE CUTANEOUS VASCULATUREJournal of Investigative Dermatology, Vol. 69, No. 1Possible feed-back inhibition of noradrenaline release by purine compoundsNaunyn-Schmiedeberg's Archives of Pharmacology, Vol. 297, No. 1Reflex control of the peripheral circulationProgress in Cardiovascular Diseases, Vol. 18, No. 5Pharmacology of pulmonary blood vesselsPharmacology & Therapeutics. Part B: General and Systematic Pharmacology, Vol. 2, No. 2Purinergic TransmissionA VASODILATOR INNERVATION TO THE CENTRAL ARTERY OF THE RABBIT EAR19 July 2012 | British Journal of Pharmacology, Vol. 52, No. 1Reflex regulation of peripheral blood flow during lung hyperinflationThe American Journal of Cardiology, Vol. 29, No. 5Molecular Inflammation Of The SkinJournal of Investigative Dermatology, Vol. 57, No. 4 More from this issue > Volume 219Issue 5November 1970Pages 1451-1457 Copyright & PermissionsCopyright © 1970 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1970.219.5.1451PubMed5473134History Published online 1 November 1970 Published in print 1 November 1970 Metrics

Chemoreflexes from the heart and lungs.

Chemoreflexes from the heart and lungs.