Journal articles: 'Rostral ventrolateral medulla'

1

McCall, R. B. "GABA-mediated inhibition of sympathoexcitatory neurons by midline medullary stimulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 255, no. 4 (October 1, 1988): R605—R615. http://dx.doi.org/10.1152/ajpregu.1988.255.4.r605.

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The present investigation determined whether the effects of electrical stimulation of depressor sites in midline medullary raphe nuclei were a result of inhibition of sympathoexcitatory medullospinal neurons in the rostral ventrolateral medulla of anesthetized cats. Electrical stimulation of the raphe inhibited inferior cardiac sympathetic activity. Microinjections of glutamate mimicked the effects of electrical stimulation. Electrical stimulation inhibited sympathoexcitatory neurons in the rostral ventrolateral medulla. The onset of the sympathoinhibition recorded from the inferior cardiac nerve (72 ms) was equal to the sum of the onset latency of the sympathoexcitatory response elicited from the rostral ventrolateral medulla (49 ms) plus the conduction time in the raphe to rostral ventrolateral sympathoinhibitory pathway (23 ms). Raphe stimulation excited a second set of neurons in the rostral ventrolateral medulla with an onset of 21 ms. Microiontophoretically applied bicuculline increased the discharge of sympathoexcitatory neurons and blocked the raphe-evoked inhibition. Iontophoretic glutamate excited sympathoexcitatory neurons but failed to antagonize raphe-elicited inhibition. These data suggest that neuronal elements in medullary raphe nuclei tonically inhibit sympathoexcitatory medullospinal neurons in the rostral ventrolateral medulla by activating closely adjacent gamma-aminobutyric acid (GABA) interneurons.

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Bergamaschi, Cássia T., Ruy R. Campos, and Oswaldo U. Lopes. "Rostral Ventrolateral Medulla." Hypertension 34, no. 4 (October 1999): 744–47. http://dx.doi.org/10.1161/01.hyp.34.4.744.

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Li, Y. W., Z. J. Gieroba, R. M. McAllen, and W. W. Blessing. "Neurons in rabbit caudal ventrolateral medulla inhibit bulbospinal barosensitive neurons in rostral medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 1 (July 1, 1991): R44—R51. http://dx.doi.org/10.1152/ajpregu.1991.261.1.r44.

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We made extracellular recordings from 104 spinally projecting neurons in the rostral ventrolateral medulla of urethan-anesthetized rabbits to test whether inhibitory vasomotor neurons in the caudal ventrolateral medulla act by inhibiting rostral sympathoexcitatory neurons. The median conduction velocity was 8.3 m/s, and the median discharge rate was 2.9 spikes/s. Raising arterial pressure with intravenous phenylephrine inhibited 88% of 77 neurons tested. The remaining units were excited. Lowering arterial pressure with nitroprusside excited 90% of 30 neurons tested. Remaining units were unaffected. Ninety-one percent of 58 rostral neurons inhibited by phenylephrine were also inhibited by injection of L-glutamate into the caudal ventrolateral medulla and 81% of 43 tested were excited by caudal injection of gamma-aminobutyric acid. These results confirm our suggestion [Brain Res. 253: 161-171, 1982; Am. J. Physiol. 254 (Heart Circ. Physiol. 23): H686-H692, 1988] and the findings of S. K. Agarwal, A. J. Gelsema, and F. R. Calaresu [Am. J. Physiol. 257 (Regulatory Integrative Comp. Physiol. 26): R265-R270, 1989]. The depressor neurons in the caudal medulla act substantially by inhibition of spinally projecting sympathoexcitatory neurons in the rostral medulla. All rostral units excited by phenylephrine were also excited by injections of L-glutamate into the caudal ventrolateral medulla, suggesting that some sympathoinhibition of baroreceptor and caudal medullary origin may take place in the spinal cord and be mediated by a subpopulation of rostral sympathoinhibitory neurons.

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Blessing, W. W. "Depressor neurons in rabbit caudal medulla act via GABA receptors in rostral medulla." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 4 (April 1, 1988): H686—H692. http://dx.doi.org/10.1152/ajpheart.1988.254.4.h686.

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Experiments were conducted in urethan-anesthetized rabbits to determine whether vasomotor effects elicited by activation or inhibition of the caudal ventrolateral medulla depend on gamma-aminobutyric acid (GABA)ergic, glycinergic, or alpha-adrenergic receptors in the region of the rostral ventrolateral medulla, which contains the bulbospinal sympathoexcitatory neurons. Bilateral injection of bicuculline methiodide into the rostral medulla caused a dose-related reduction in the fall in arterial pressure and in the inhibition of renal sympathetic nerve activity normally elicited by chemical stimulation of neurons in the caudal medulla using local injection of L-glutamate. When both bicuculline and muscimol were injected into the rostral medulla at the same time, resting arterial pressure was maintained at base-line levels, and the sympathoexcitatory neurons remained normally excitable by local injection of L-glutamate into the rostral medulla. In the presence of this mixed antagonist-agonist GABAergic blockade, both decreases and increases in arterial pressure elicited by excitation or inhibition of neuronal function in the caudal medulla were abolished. Similar effects were not observed after blockade of glycinergic or alpha-adrenergic receptors in the rostral ventrolateral medulla. Results suggest that the depressor neurons in the caudal ventrolateral medulla alter peripheral sympathetic vasomotor activity almost entirely by an action on GABAergic receptors in the rostral ventrolateral medulla.

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Sun, Wei, and W. Michael Panneton. "The caudal pressor area of the rat: its precise location and projections to the ventrolateral medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 3 (September 1, 2002): R768—R778. http://dx.doi.org/10.1152/ajpregu.00184.2002.

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Investigators have demonstrated pressor areas in the medullas of various species. The present study precisely localized the pressor area in the caudal medulla of the rat and determined its projections to the caudal and rostral ventrolateral medulla. The caudal medulla first was mapped grossly in rats with injections (30 nl) of glutamate (30-, 15-, and 7.5-nmol doses) placed 0.5, 1.0, and 1.5 mm caudal to the calamus scriptorius, 1.0, 1.5, and 2.0 mm lateral to the midline, and 1.8, 1.7, and 1.6 mm ventral to the dorsal medullary surface, respectively, and their arterial pressures were recorded. One of these nine injections showed significant increases in arterial pressure. We micromapped this area with a total of 27 injections of glutamate (10 nl; 5 nmol) placed 300 μm apart at 3 different dorsoventral levels. This micromapping study pinpointed the precise location of caudal pressor area (CPA) neurons in a restricted region lateral to the caudal end of the lateral reticular nucleus and ventromedial to the medullary dorsal horn near the level of the pyramidal decussation. Injections of glutamate into this spot, 1.0 mm caudal to the calamus scriptorius, 2.0 mm lateral to the midline, and 1.7 mm ventral from the dorsal surface of the medulla, induced significant increases in arterial pressure. The neuroanatomic connections of neurons in the CPA to the ventrolateral medulla were then investigated with iontophoretic injections of either the anterograde tracer biotinylated dextran amine (BDA) made into the CPA or the retrograde tracer FluoroGold (FG) injected into either the caudal or rostral ventrolateral medulla. BDA injections resulted in bouton-laden fibers throughout both caudal and rostral portions of the ventrolateral medulla. Either of the FG injections resulted in numerous spindle-shaped neurons interspersed between the longitudinal fiber bundles running through the CPA area. The proximity of the CPA neurons to the A1 catecholaminergic cell group is discussed.

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Guyenet, Patrice G., Ruth L. Stornetta, Benjamin B. Holloway, George M. P. R. Souza, and Stephen B. G. Abbott. "Rostral Ventrolateral Medulla and Hypertension." Hypertension 72, no. 3 (September 2018): 559–66. http://dx.doi.org/10.1161/hypertensionaha.118.10921.

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Min, Sun Ki, Jinyoung Oh, Taemin Kim, Ji Eun Han, Sang Won Han, and Hyun-jeung Yu. "Laterality of Skin Temperature and Magnetic Resonance Imaging in Patients with Wallenberg Syndrome." Journal of Neurosonology and Neuroimaging 13, no. 2 (December 31, 2021): 47–54. http://dx.doi.org/10.31728/jnn.2021.00101.

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Background: Recently, lateral differences in body surface temperature (BST) have been reported as a symptom of Wallenberg syndrome (WS), resulting from disturbances in the sympathetic nerve pathway. This study aimed to investigate the relationship between the laterality of BST and brain magnetic resonance imaging (MRI) findings in 12 patients with WS.Methods: BST was measured using an infrared thermal camera at 7±3 days and 90±30 days after symptom onset. The MRI findings were categorized as rostral, middle, and caudal medulla rostrocaudally and typical, ventral, large, dorsal, and lateral types in the horizontal direction.Results: MRI revealed medullary lesions on the right in five patients and on the left in seven patients. Two patients without lateralized BST had lateral caudal medullary infarction, and one patient had a dorsal middle medullary infarction. One patient with lateralized BST had a rostral medullary infarction and the other had a typical or large middle medulla infarction. Lateralized BST in patients with WS may disturb the sympathetic nervous system pathway that descends from the rostral ventrolateral medulla oblongata. Deficits in sweating and skin blood flow may cause BST laterality.Conclusion: This study showed that lateralized BST in patients with WS may be associated with disturbances in the sympathetic nervous pathway descending from the rostral ventrolateral medulla. These results support the assumption that autonomic dysfunction may be related to abnormal sensory symptoms in patients with WS.

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Guyenet, P. G., R. A. Darnall, and T. A. Riley. "Rostral ventrolateral medulla and sympathorespiratory integration in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 259, no. 5 (November 1, 1990): R1063—R1074. http://dx.doi.org/10.1152/ajpregu.1990.259.5.r1063.

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The respiratory modulation of the lumbar sympathetic nerve discharge (LSND) was examined in halothane-anesthetized, paralyzed, and vagotomized rats by means of phrenic nerve discharge (PND)-triggered histograms. The respiratory modulation was 1) proportional to PND amplitude during chemoreceptor activation with CO2 and 2) reduced at elevated arterial pressure. Bilateral injections of bicuculline [gamma-aminobutyric acid (GABA)A receptor antagonist, n = 5] into the rostral ventrolateral medulla (RVLM), but not into medullary raphe, reversibly increased mean arterial pressure (MAP) and resting LSND, decreased the baroreflex, reduced PND amplitude and central respiratory rate, and greatly magnified the respiratory modulation of LSND. Injections of strychnine (glycine receptor antagonist, n = 5) or phaclofen (GABAB receptor antagonist, n = 2) into RVLM were without effect. Injections of kynurenic acid (excitatory amino acid receptor antagonist) into RVLM (n = 8), but not raphe (n = 3), reduced PND amplitude, increased central respiratory rate, reduced MAP, elevated resting LSND slightly, and greatly reduced the respiratory modulation of LSND. These data suggest that the rostral tip of the ventrolateral medulla represents a critical link between the central respiratory rhythm generator and the vasomotor outflow. Also, it indicates that the respiratory modulation of SND does not involve a gating of the activity of the medullary neurons that convey baroreceptor information to RVLM sympathoexcitatory neurons.

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Vizzard, M. A., A. Standish, and W. S. Ammons. "Renal afferent input to the ventrolateral medulla of the cat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 2 (August 1, 1992): R412—R422. http://dx.doi.org/10.1152/ajpregu.1992.263.2.r412.

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Experiments were performed to determine if information from the kidneys projects to the rostral ventrolateral medulla. Extracellular action potentials were recorded from 148 cells within the rostral ventrolateral medulla of alpha-chloralose-anesthetized cats. Cells within the rostral ventrolateral medulla were tested for responses to electrical stimulation of both left and right renal nerves. Electrical stimulation of renal nerves excited 144 cells (97.3%) and inhibited 4. The majority of cells received either bilateral or contralateral renal nerve input. Cells with bilateral renal nerve input responded to contralateral renal nerve stimulation with a significantly greater number of impulses compared with ipsilateral renal nerve stimulation (P less than 0.05). All cells but one responding to renal nerve stimulation had convergent somatic input. Comparisons between thresholds for cell responses and activation thresholds for the A and C volleys of the compound action potential recorded in the least splanchnic nerve revealed that 44 cells required activation of A delta-fibers, and 12 cells required activation of both A delta- and C-fibers. A conditioning stimulus applied to renal nerves on one side significantly decreased the response elicited by a test stimulus applied to the renal nerves on the opposite side for at least 300 ms (P less than 0.05). The demonstration that an afferent connection exists between the kidneys and the ventrolateral medulla suggests that the rostral ventrolateral medulla may play a role in mediating supraspinal reflexes of renal origin.

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10

Steinbacher, B. C., and B. J. Yates. "Processing of vestibular and other inputs by the caudal ventrolateral medullary reticular formation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 4 (October 1, 1996): R1070—R1077. http://dx.doi.org/10.1152/ajpregu.1996.271.4.r1070.

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Lesions of the lateral medullary reticular formation caudal to the obex abolish vestibulosympathetic and somatosympathetic responses; this area also contains neurons that mediate baroreceptor reflexes. Recordings were made from neurons in the caudal medullary reticular formation of cats that were decerebrate or anesthetized using alpha-chloralose-urethan to determine whether common neurons responded to electrical stimulation of vestibular and hindlimb afferents and had cardiac-related (i.e., baroreceptor) inputs. Many neurons in the ventrolateral portion of the caudal reticular formation received labyrinthine inputs, and they were interspersed with neurons that received baroreceptor signals. However, virtually none of the units received convergent baroreceptor and vestibular inputs, suggesting that separate pathways from the caudal ventrolateral medulla mediate baroreceptor and vestibulosympathetic reflexes. Furthermore, the neurons that received labyrinthine signals could not be antidromically activated from electrodes inserted into the rostral ventrolateral medulla, which is known to mediate vestibulosympathetic responses; thus an indirect pathway must convey vestibular inputs from the caudal to rostral medullary reticular formation. Over 75% of both neurons with baroreceptor inputs and cells with vestibular signals responded to sciatic nerve stimulation, suggesting that more than one pathway from the caudal medulla may mediate somatosympathetic responses.

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11

Beluli, D. J., and L. C. Weaver. "Differential control of renal and splenic nerves without medullary topography." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 4 (April 1, 1991): H1072—H1079. http://dx.doi.org/10.1152/ajpheart.1991.260.4.h1072.

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A previous study in our laboratory showed that pharmacological blockade of neurons in the rostral ventrolateral medulla has greater influence on the electrical activity of renal than splenic nerves (K. Hayes and L. C. Weaver, J. Physiol. Lond. 428: 371-385, 1990). This differential control of sympathetic nerves innervating different organs may be due to viscerotopic representation of the kidney and spleen within medullary neurons that control the vasculature. To search for this topographical organization, 15 nl (2.5 nmol) of the excitatory amino acid DL-homocysteic acid (DLH) was microinjected into the ventrolateral medulla (VLM) of rats anesthetized with urethan. No distinct viscerotopic organization was found in the rostral or caudal VLM. However, renal nerve responses were consistently greater than splenic by a fixed proportion. In summary, stimulation of rostral and caudal VLM neurons causes differential renal and splenic excitatory responses, but mechanisms providing this selective control do not involve spatial organization of neuronal groups in the VLM.

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Smith, J. K., and K. W. Barron. "GABAergic responses in ventrolateral medulla in spontaneously hypertensive rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 2 (February 1, 1990): R450—R456. http://dx.doi.org/10.1152/ajpregu.1990.258.2.r450.

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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)

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Ma, Anyun, Lie Gao, Ahmed M. Wafi, Li Yu, Tara Rudebush, Wenxian Zhou, and Irving H. Zucker. "Overexpression of Central ACE2 (Angiotensin-Converting Enzyme 2) Attenuates the Pressor Response to Chronic Central Infusion of Ang II (Angiotensin II)." Hypertension 76, no. 5 (November 2020): 1514–25. http://dx.doi.org/10.1161/hypertensionaha.120.15681.

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We investigated the mechanism by which ACE2 (angiotensin-converting enzyme 2) overexpression alters neurohumoral outflow and central oxidative stress. Nrf2 (nuclear factor [erythroid-derived 2]-like 2) is a master antioxidant transcription factor that regulates cytoprotective and antioxidant genes. We hypothesized that upregulation of central ACE2 inhibits the pressor response to Ang II (angiotensin II) by reducing reactive oxygen species through a Nrf2/antioxidant enzyme–mediated mechanism in the rostral ventrolateral medulla. Synapsin human Angiotensin Converting Enzyme 2 positive (SynhACE2 +/+ ) mice and their littermate controls synhACE2 −/− were used to evaluate the consequence of intracerebroventricular infusion of Ang II. In control mice, Ang II infusion evoked a significant increase in blood pressure and norepinephrine excretion, along with polydipsia and polyuria. The pressor effect of central Ang II was completely blocked in synhACE2 +/+ mice. Polydipsia, norepinephrine excretion, and markers of oxidative stress in response to central Ang II were also reduced in synhACE2 +/+ mice. The MasR (Mas receptor) agonist Ang 1–7 and blocker A779 had no effects on blood pressure. synhACE2 +/+ mice showed enhanced expression of Nrf2 in the rostral ventrolateral medulla which was blunted following Ang II infusion. Ang II evoked nuclear translocation of Nrf2 in cultured Neuro 2A (N2A) cells. In synhACE2 −/− mice, the central Ang II pressor response was attenuated by simultaneous intracerebroventricular infusion of the Nrf2 activator sulforaphane; blood pressure was enhanced by knockdown of Nrf2 in the rostral ventrolateral medulla in Nrf2 floxed (Nrf2 f/f ) mice. These data suggest that the hypertensive effects of intracerebroventricular Ang II are attenuated by selective overexpression of brain synhACE2 and may be mediated by Nrf2-upregulated antioxidant enzymes in the rostral ventrolateral medulla.

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Varner, K. J., E. C. Vasquez, and M. J. Brody. "Lesions in rostral ventromedial or rostral ventrolateral medulla block neurogenic hypertension." Hypertension 24, no. 1 (July 1994): 91–96. http://dx.doi.org/10.1161/01.hyp.24.1.91.

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Cravo, S. L., S. F. Morrison, and D. J. Reis. "Differentiation of two cardiovascular regions within caudal ventrolateral medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 4 (October 1, 1991): R985—R994. http://dx.doi.org/10.1152/ajpregu.1991.261.4.r985.

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The caudal ventrolateral medulla (CVLM) plays a significant role in the regulation of sympathetic nerve activity (SNA) and arterial pressure; however, the use of lesions to examine its role in mediating baroreceptor reflex control of SNA has yielded discrepant results. We hypothesize that this may have arisen from anatomic segregation of neurons within the CVLM that subserve different functions in sympathetic control. Thus we used microinjections of the excitotoxic agent kainic acid (200 pmol in 20 nl) to determine the effects of inactivation of neuronal cell bodies in a rostral and a caudal subregion of the CVLM on SNA, arterial pressure, and baroreceptor reflex function in urethan-anesthetized rats. Interruption of neuronal activity in the rostral CVLM (sites from 0.6 mm caudal to 0.5 mm rostral to the rostral border of the lateral reticular nucleus) elevated SNA (post-kainic acid 214% of control) and arterial pressure (+34 mmHg) and eliminated the inhibition of splanchnic SNA evoked by either aortic nerve stimulation or the pressor response to intravenous norepinephrine. In addition, the cardiac-related component of spontaneous SNA was abolished as judged from post-R wave averages and from power spectral analysis. In contrast, although a similar disruption of neuronal activity in the caudal CVLM (sites 0.0-0.6 mm rostral to the caudal border of the lateral reticular nucleus) produced a comparable increase in spontaneous SNA (post-kainic acid 196% of control) and arterial pressure (+20 mmHg), it was without effect on the ability of the baroreceptor reflex to inhibit SNA, and it enhanced the synchronization of the spontaneous bursts in SNA to the cardiac cycle. Our results suggest an organization of the CVLM in which neurons in its rostral portion are required for an effective baroreceptor reflex, whereas those in the caudal CVLM serve to limit SNA and blood pressure independent of the baroreceptor reflex.

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Li, J., G. A. Hand, J. T. Potts, L. B. Wilson, and J. H. Mitchell. "c-Fos expression in the medulla induced by static muscle contraction in cats." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 1 (January 1, 1997): H48—H56. http://dx.doi.org/10.1152/ajpheart.1997.272.1.h48.

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In this study, we examined Fos-like immunoreactivity (FLI) in the medulla after static muscle contraction induced by stimulation of L7 and S1 ventral roots of the spinal cord in anesthetized cats. The results show that FLI increases in the lateral reticular nucleus, nucleus of the solitary tract, lateral tegmental field, vestibular nucleus, subretrofacial nucleus, and A1 region of the medulla in comparison with these same areas in sham-operated animals (P < 0.05 in each region). In the rostral ventrolateral medulla, FLI distribution in neurons containing phenylethanolamine-N-methyltransferase (PNMT, the synthetic enzyme for epinephrine) was also observed utilizing double-labeling methods. The majority of neurons with PNMT also expressed FLI (66 +/- 4%). These data are in contrast to the results from sham-operated animals showing that 24 +/- 3% of the neurons costained with PNMT (P < 0.05). Our findings indicate that expression of FLI can be used to identify neurons activated during static muscle contraction and support previous studies implicating the ventrolateral medulla as a critical region for expression of the exercise pressor reflex. Furthermore, neurons in the rostral ventrolateral medulla containing PNMT were activated during static muscle contraction.

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Blessing, WW. "Inhibitory Vasomotor Neurons in the Caudal Ventrolateral Medulla Oblongata." Physiology 6, no. 3 (June 1, 1991): 139–41. http://dx.doi.org/10.1152/physiologyonline.1991.6.3.139.

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Tonically active, probably GABAergic, neurons in the caudal ventrolateral medulla oblongata decrease sympathetic vasomotor tone by directly inhibiting sympathoexcitatory premotor neurons in the rostral medulla. These caudal inhibitory vasomotor neurons may constitute the inhibitory link in the central baroreceptor-vasomotor pathway.

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Guyenet, Patrice G., and Ruth L. Stornetta. "Rostral ventrolateral medulla, retropontine region and autonomic regulations." Autonomic Neuroscience 237 (January 2022): 102922. http://dx.doi.org/10.1016/j.autneu.2021.102922.

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Guyenet, Patrice G., Ruth L. Stornetta, Ann M. Schreihofer, Nicole M. Pelaez, Abdallah Hayar, Sue Aicher, and Ida J. Llewellyn-Smith. "Opioid Signalling In The Rat Rostral Ventrolateral Medulla." Clinical and Experimental Pharmacology and Physiology 29, no. 3 (March 2002): 238–42. http://dx.doi.org/10.1046/j.1440-1681.2002.03636.x.

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Hilaire, Gérard, Céline Bou, and Roger Monteau. "Rostral ventrolateral medulla and respiratory rhythmogenesis in mice." Neuroscience Letters 224, no. 1 (March 1997): 13–16. http://dx.doi.org/10.1016/s0304-3940(97)13458-9.

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Siddall, P. J., R. A. L. Dampney, and J. W. Polson. "Descending antinociceptive pathways in the rostral ventrolateral medulla." Pain 41 (January 1990): S447. http://dx.doi.org/10.1016/0304-3959(90)93009-m.

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Abbott, Stephen B. G., and Paul M. Pilowsky. "Galanin microinjection into rostral ventrolateral medulla of the rat is hypotensive and attenuates sympathetic chemoreflex." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 4 (April 2009): R1019—R1026. http://dx.doi.org/10.1152/ajpregu.90885.2008.

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Galanin is present in neurons in the brain that are important in the control of arterial pressure, and intracisternal administration of galanin evokes hypotension, but the site of action is unknown. In urethane-anesthetized, vagotomized mechanically ventilated Sprague-Dawley rats ( n = 34), we investigated the effects of microinjecting galanin (1 mM, 50 nl, 50 pmol) into the rostral ventrolateral medulla on resting splanchnic sympathetic nerve activity, arterial pressure, heart rate, and phrenic nerve activity. Second, we determined the effect of microinjecting galanin into the rostral ventrolateral medulla on the cardiovascular response to stimulation of central and peripheral chemoreceptors, arterial baroreceptors, and the somatosympathetic reflex. Galanin caused a prolonged reduction in resting splanchnic sympathetic nerve activity (−37.0 ± 7.2% of baseline), mean arterial pressure (−17.0 ± 3.5 mmHg), and heart rate (−25.0 ± 9.1 beats/min). Galanin increased the sympathoinhibitory response to aortic depressor nerve stimulation by 51.8%, had no effect on the somatosympathetic reflex, and markedly attenuated the effect of hypercapnia and hypoxia on arterial pressure (by 65% and 92.4% of control, respectively). These results suggest a role for galanin neurotransmission in the integration of the cardiovascular responses to hypoxia, hypercapnia, and the sympathetic baroreflex in the rostral ventrolateral medulla. The data suggest that galanin may be an important peptide in the homeostatic regulation of chemosensory reflexes.

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Chalmers, John, Vimal Kapoor, Eric Mills, Jane Minson, Margaret Morris, Paul Pilowsky, and Malcolm West. "Do pressor neurons in the ventrolateral medulla release amines and neuropeptides?" Canadian Journal of Physiology and Pharmacology 65, no. 8 (August 1, 1987): 1598–604. http://dx.doi.org/10.1139/y87-251.

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Activation of neurons arising in the rostral ventrolateral medulla evokes a pressor response in the rat and the rabbit. This region of the medulla gives rise to bulbospinal neurons containing many different neurotransmitters, including amines such as adrenaline, noradrenaline and serotonin, and neuropeptides such as substance P and neuropeptide Y. Colocalization of amines and neuropeptides has been described in some neurons descending from the rostral ventrolateral medulla. In this paper we discuss the evidence that bulbospinal serotonin-containing neurons (B3) and adrenaline-containing neurons (C1) arising from this part of the medulla exert pressor effects by distinct central pathways and conclude that they do. We also consider the possibility that the pressor effects of activating these two groups of neurons are associated with release of neuropeptides and highlight evidence that substance P is released into the spinal cord by activation of descending serotonin-containing neurons, while neuropeptide Y may be released by activation of bulbospinal adrenaline-containing neurons.

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Gieroba, Z. J., Y. W. Li, and W. W. Blessing. "Characteristics of caudal ventrolateral medullary neurons antidromically activated from rostral ventrolateral medulla in the rabbit." Brain Research 582, no. 2 (June 1992): 196–207. http://dx.doi.org/10.1016/0006-8993(92)90133-t.

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Lorenzo-Martín, L. Francisco, Mauricio Menacho-Márquez, Salvatore Fabbiano, Omar Al-Massadi, Antonio Abad, Sonia Rodríguez-Fdez, María A. Sevilla, et al. "Vagal afferents contribute to sympathoexcitation-driven metabolic dysfunctions." Journal of Endocrinology 240, no. 3 (March 2019): 483–96. http://dx.doi.org/10.1530/joe-18-0623.

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Multiple crosstalk between peripheral organs and the nervous system are required to maintain physiological and metabolic homeostasis. Using Vav3-deficient mice as a model for chronic sympathoexcitation-associated disorders, we report here that afferent fibers of the hepatic branch of the vagus nerve are needed for the development of the peripheral sympathoexcitation, tachycardia, tachypnea, insulin resistance, liver steatosis and adipose tissue thermogenesis present in those mice. This neuronal pathway contributes to proper activity of the rostral ventrolateral medulla, a sympathoregulatory brainstem center hyperactive in Vav3−/− mice. Vagal afferent inputs are also required for the development of additional pathophysiological conditions associated with deregulated rostral ventrolateral medulla activity. By contrast, they are dispensable for other peripheral sympathoexcitation-associated disorders sparing metabolic alterations in liver.

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Badoer, Emilio, Michael J. McKinley, Brian J. Oldfield, and Robin M. McAllen. "Localization of barosensitive neurons in the caudal ventrolateral medulla which project to the rostral ventrolateral medulla." Brain Research 657, no. 1-2 (September 1994): 258–68. http://dx.doi.org/10.1016/0006-8993(94)90975-x.

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Duffin, J., K. Ezure, and J. Lipski. "Breathing Rhythm Generation: Focus on the Rostral Ventrolateral Medulla." Physiology 10, no. 3 (June 1, 1995): 133–40. http://dx.doi.org/10.1152/physiologyonline.1995.10.3.133.

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Current knowledge about the generation of breathing rhythm is reviewed. The respiratory neurophysiology of the medulla and particularly its rostral ventrolateral part as well as the major hypotheses of breathing rhythm generation are discussed. A model incorporating recent concepts is presented.

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Stornetta, R. L., S. F. Morrison, D. A. Ruggiero, and D. J. Reis. "Neurons of rostral ventrolateral medulla mediate somatic pressor reflex." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 2 (February 1, 1989): R448—R462. http://dx.doi.org/10.1152/ajpregu.1989.256.2.r448.

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

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Jung, Young Ik, Mun Kyung Sunwoo, Hee Jin Lee, Jeong Hee Seo, and Jeongyeon Kim. "Orthostatic hypotension with meningoencephalitis involving the rostral ventrolateral medulla." Annals of Clinical Neurophysiology 21, no. 1 (2019): 66. http://dx.doi.org/10.14253/acn.2019.21.1.66.

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J. Reis, Donald, David A. Ruggiero, and Shaun F. Morrison. "The CI Area of the Rostral Ventrolateral Medulla Oblongata." American Journal of Hypertension 2, no. 12_Pt_2 (December 1989): 363S—374S. http://dx.doi.org/10.1093/ajh/2.12.363s.

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Morimoto, Satoshi, Susumu Sasaki, Shigeyuki Miki, Tetsuyoshi Kawa, Hiroshi Itoh, Tetsuo Nakata, Kazuo Takeda, Masao Nakagawa, Shoji Naruse, and Tomoho Maeda. "Pulsatile Compression of the Rostral Ventrolateral Medulla in Hypertension." Hypertension 29, no. 1 (January 1997): 514–18. http://dx.doi.org/10.1161/01.hyp.29.1.514.

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32

Rentero, N., N. Bruandet, and L. Quintin. "Rostral ventrolateral medulla catechol involvement upon sino-aortic deafferentation." Life Sciences 68, no. 2 (December 2000): 177–89. http://dx.doi.org/10.1016/s0024-3205(00)00927-9.

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33

Dempsey, B., A. Turner, S. Le, A. Allen, A. Goodchild, and S. McMullan. "The connectome of rostral ventrolateral medulla sympathetic premotor neurons." Autonomic Neuroscience 192 (November 2015): 48. http://dx.doi.org/10.1016/j.autneu.2015.07.401.

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Naraghi, Ramin, Michael R. Gaab, Gerhard F. Walter, and Berthold Kleineberg. "Arterial hypertension and neurovascular compression at the ventrolateral medulla." Journal of Neurosurgery 77, no. 1 (July 1992): 103–12. http://dx.doi.org/10.3171/jns.1992.77.1.0103.

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✓ Intraoperative observations and animal experiments suggest that neurovascular compression at the left ventrolateral medulla is a possible etiological factor in essential hypertension. In pursuing this hypothesis, the authors examined the neurovascular relations in the posterior cranial fossa of 24 patients with essential hypertension, of 10 with renal hypertension, and of 21 normotensive control patients. Artificial perfusion of the vessels and microsurgical investigations during autopsy identified the vascular relations at the brain stem and at the root entry zone of the caudal cranial nerves. There was no evidence of neurovascular compression at the ventrolateral medulla on the left side in any patient from the control group or among those with renal hypertension. Two normotensive patients had neurovascular compression at the right ventrolateral medulla by the posterior inferior cerebellar artery. In contrast, all patients with essential hypertension had definite neurovascular compression at the left ventrolateral medulla. Additional compression of the right side was seen in three of these patients. Based on the anatomical appearance, it was possible to define three distinct types of neurovascular compression at the ventrolateral medulla. Common to all three types is the compression of the medulla oblongata at its rostral part just caudal to the pontomedullary junction and lateral to the olive in the retro-olivary sulcus. Comparative histopathological study of the microsurgically examined brain-stem specimens revealed no differences between patients with essential hypertension, those with renal hypertension, and normal controls. There was a structural integrity at the site of neurovascular compression at the ventrolateral medulla. The microanatomical findings of this study show that neurovascular relations at the ventrolateral medulla in essential hypertension give rise to pulsatile compression on the left. This supports Jannetta's hypothesis of neurovascular compression at the left ventrolateral medulla as an etiology of essential hypertension.

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Terui, Naohito, Noboru Masuda, Yuka Saeki, Naohiro Koshiya, and Mamoru Kumada. "Electrophysiological evidence that neurons in the caudal ventrolateral medulla inhibit sympathoexcitatory neurons in the rostral ventrolateral medulla." Neuroscience Research Supplements 15 (January 1990): S20. http://dx.doi.org/10.1016/0921-8696(90)90093-i.

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Terui, Naohito, Noboru Masuda, Yuka Saeki, Naohiro Koshiya, and Mamoru Kumada. "Electrophysiological evidence that neurons in the caudal ventrolateral medulla inhibit sympathoexcitatory neurons in the rostral ventrolateral medulla." Neuroscience Research Supplements 11 (January 1990): S20. http://dx.doi.org/10.1016/0921-8696(90)90516-6.

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Li, P. "Modulatory Effect of Somatic Inputs on Medullary Cardiovascular Neuronal Function." Physiology 6, no. 2 (April 1, 1991): 69–72. http://dx.doi.org/10.1152/physiologyonline.1991.6.2.69.

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Inhibition of somatic inputs on pressor response and arrhythmia is due to activating opiate receptors in the rostral ventrolateral medulla (rVLM), while its pressor response and blocking effect on bradycardia are due to activating cholinergic receptor in rVLM.

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Lindsey, B. G., L. S. Segers, K. F. Morris, Y. M. Hernandez, S. Saporta, and R. Shannon. "Distributed actions and dynamic associations in respiratory-related neuronal assemblies of the ventrolateral medulla and brain stem midline: evidence from spike train analysis." Journal of Neurophysiology 72, no. 4 (October 1, 1994): 1830–51. http://dx.doi.org/10.1152/jn.1994.72.4.1830.

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1. Considerable evidence indicates that neurons in the brain stem midline and ventrolateral medulla participate in the control of breathing. This work was undertaken to detect and evaluate evidence for functional links that coordinate the parallel operations of neurons distributed in these two domains. 2. Data were from 51 Dial-urethan-anesthetized, bilaterally vagotomized, paralyzed, artificially ventilated cats. Planar arrays of tungsten microelectrodes were used to monitor simultaneously spike trains in two or three of the following regions: n. raphe obscurus-n. raphe pallidus, n. raphe magnus, rostral ventrolateral medulla, and caudal ventrolateral medulla. Efferent phrenic nerve activity was recorded to indicate the phases of the respiratory cycle. Electrodes in the ventral spinal cord (C3) were used in antidromic stimulation tests for spinal projections of neurons. 3. Spike trains of 1,243 neurons were tested for respiratory modulated firing rates with cycle-triggered histograms and an analysis of variance with the use of a subjects-by-treatments experimental design. Functional associations were detected and evaluated with cross-correlograms, snowflakes, and the gravity method. 4. Each of 2,310 pairs of neurons studied included one neuron monitored within 0.6 nm of the brain stem midline and a second cell recorded in the ventrolateral medulla; 117 of these pairs (5%) included a neuron with a spinal projection, identified with antidromic stimulation methods, that extended to at least the third cervical segment. Short-time scale correlations were detected in 110 (4.7%) pairs of neurons. Primary cross-correlogram features included 40 central peaks, 47 offset peaks, 4 central troughs, and 19 offset troughs. 5. In 14 data sets, multiple short-time scale correlations were found among three or more simultaneously recorded neurons distributed between both midline and ventrolateral domains. The results suggested that elements of up to three layers of interneurons were monitored simultaneously. Evidence for concurrent serial and parallel regulation of impulse synchrony was detected. Gravitational representations demonstrated respiratory-phase dependent synchrony among neurons distributed in both brain stem regions. 6. The results support a model of the brain stem respiratory network composed of coordinated distributed subassemblies and provide evidence for several hypotheses. 1) Copies of respiratory drive information from rostral ventrolateral medullary (RVLM) respiratory neurons are transmitted to midline neurons. 2) Midline neurons act on respiratory-related neurons in the RVLM to modulate phase timing. 3) Impulse synchrony of midline neurons is influenced by concurrent divergent actions of both midline and ventrolateral neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

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39

Coleman, Matthew J., and Roger A. L. Dampney. "Sympathoinhibition evoked from caudal midline medulla is mediated by GABA receptors in rostral VLM." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 2 (February 1, 1998): R318—R323. http://dx.doi.org/10.1152/ajpregu.1998.274.2.r318.

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The present study was performed to determine whether the powerful depressor and sympathoinhibitory response that can be evoked from neurons in the caudal midline medulla is mediated by γ-aminobutyric acidergic (GABAergic) inhibition of sympathoexcitatory neurons in the rostral part of the ventrolateral medulla (VLM). In anesthetized barointact and barodenervated rabbits, bilateral microinjections of bicuculline into sympathoexcitatory sites in the rostral VLM resulted in a sustained increase in renal sympathetic nerve activity and abolished or reversed the depressor and sympathoinhibitory response evoked by glutamate microinjection into the caudal midline medulla. By contrast, the sympathoinhibitory response evoked from the caudal midline medulla persisted when the background level of renal sympathetic nerve activity was reflexly raised by baroreceptor unloading. The results indicate that 1) the depressor and sympathoinhibitory response evoked by stimulation of neurons in the caudal midline medulla is mediated by a GABAergic synapse in the rostral VLM and 2) there are also sympathoexcitatory neurons in the caudal midline medulla whose presence is revealed by blockade of the more powerful sympathoinhibitory response.

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Chen, Chiung-Tong, Ling-Ling Hwang, Jaw-Kang Chang, and Nae J. Dun. "Pressor effects of orexins injected intracisternally and to rostral ventrolateral medulla of anesthetized rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 3 (March 1, 2000): R692—R697. http://dx.doi.org/10.1152/ajpregu.2000.278.3.r692.

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Orexin A and B, two recently isolated hypothalamic peptides, have been reported to increase food consumption upon intracerebroventricular injections in rats. In addition to the hypothalamus, orexin A-immunoreactive fibers have been observed in several areas of the medulla that are associated with cardiovascular functions. The present study was undertaken to evaluate the hypothesis that orexins may influence cardiovascular response by interacting with neurons in the medulla. Intracisternal injections of orexins A (0.0056–7.0 nmol) or B (0.028–0.28 nmol) dose dependently increased mean arterial pressure (MAP) by 4–27 mmHg and heart rate (HR) by 26–80 beats/min in urethan-anesthetized rats, with orexin A being more effective in this regard. MAP and HR were not changed by intravenous injection of orexins at higher concentrations. Microinjection of orexin A (14 pmol/50.6 nl) to the rostral ventrolateral medulla, which was confirmed by histological examination, increased MAP and HR. Our results indicate that, in addition to a role in positive feeding behavior, orexins may enhance cardiovascular response via an action on medullary neurons.

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Nattie, E. E., J. Wood, A. Mega, and W. Goritski. "Rostral ventrolateral medulla muscarinic receptor involvement in central ventilatory chemosensitivity." Journal of Applied Physiology 66, no. 3 (March 1, 1989): 1462–70. http://dx.doi.org/10.1152/jappl.1989.66.3.1462.

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The muscarinic receptor antagonist atropine (105 mM) dramatically decreased the response to increased CO2 when applied by cotton pledgets to the rostral ventrolateral medulla ventilatory chemosensitive area in anesthetized, paralyzed, vagotomized, glomectomized, and servoventilated cats with integrated phrenic nerve activity used as respiratory center output. Lower dose atropine (4.4 mM) and the M1-muscarinic receptor subtype antagonist pirenzepine (10 mM) also significantly decreased the mean CO2 response slope 48.3 +/- 6.2 and 40.7 +/- 6.0% (SE), respectively, and significantly decreased the maximum response value 26.3 +/- 8.1 and 19.2 +/- 3.2%, respectively, without significant effects on blood pressure or on the phrenic response to carotid sinus nerve stimulation. The M2-muscarinic receptor subtype antagonist AF-DX 116 (10 mM) had no significant effect on phrenic output or blood pressure. Application of carbachol (10 mM) at the rostral area augmented eucapnic phrenic output and the maximum value of the CO2 response but decreased the initial slope, effects blocked by atropine. Carbachol also decreased the response to carotid sinus nerve stimulation, suggesting that the system was saturated by carbachol stimulation. Muscarinic cholinergic receptors accessible to surface application at the rostral ventrolateral medulla antagonized by pirenzepine but not AF-DX 116 appear to be involved in the central chemoreceptor process.

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Barman, Susan M. "2019 Ludwig Lecture: Rhythms in sympathetic nerve activity are a key to understanding neural control of the cardiovascular system." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 318, no. 2 (February 1, 2020): R191—R205. http://dx.doi.org/10.1152/ajpregu.00298.2019.

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This review is based on the Carl Ludwig Distinguished Lecture, presented at the 2019 Experimental Biology Meeting in Orlando, FL, and provides a snapshot of >40 years of work done in collaboration with the late Gerard L. Gebber and colleagues to highlight the importance of considering the rhythmic properties of sympathetic nerve activity (SNA) and brain stem neurons when studying the neural control of autonomic regulation. After first providing some basic information about rhythms, I describe the patterns and potential functions of rhythmic activity recorded from sympathetic nerves under various physiological conditions. I review the evidence that these rhythms reflect the properties of central sympathetic neural networks that include neurons in the caudal medullary raphe, caudal ventrolateral medulla, caudal ventrolateral pons, medullary lateral tegmental field, rostral dorsolateral pons, and rostral ventrolateral medulla. The role of these brain stem areas in mediating steady-state and reflex-induced changes in SNA and blood pressure is discussed. Despite the common appearance of rhythms in SNA, these oscillatory characteristics are often ignored; instead, it is common to simply quantify changes in the amount of SNA to make conclusions about the function of the sympathetic nervous system in mediating responses to a variety of stimuli. This review summarizes work that highlights the need to include an assessment of the changes in the frequency components of SNA in evaluating the cardiovascular responses to various manipulations as well as in determining the role of different brain regions in the neural control of the cardiovascular system.

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Schobel, Hans P., Helga Frank, Ramin Naraghi, Helmut Geiger, Elmar Titz, and Karsten Heusser. "Hypertension in Patients with Neurovascular Compression Is Associated with Increased Central Sympathetic Outflow." Journal of the American Society of Nephrology 13, no. 1 (January 2002): 35–41. http://dx.doi.org/10.1681/asn.v13135.

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ABSTRACT. Recent data suggest a causal relationship between essential hypertension and neurovascular compression (NVC) at the rostral ventrolateral medulla. An increase of central sympathetic outflow might be an underlying pathomechanism. The sympathetic nerve activity to muscle was recorded in 21 patients with hypertension with NVC (NVC+ group) and in 12 patients with hypertension without NVC (NVC− group). Heart rate variability, respiratory activity, BP, and central venous pressure at rest and during unloading of cardiopulmonary baroreceptors with lower-body negative pressure and during a cold pressor test were also measured. Resting sympathetic nerve activity to muscle was twice as high in the NVC+ group compared with the NVC− group (34 ± 22 versus 18 ± 6 bursts/min; P < 0.05). Resting heart rate (P = 0.06) and low- to high-frequency power ratio values (P = NS) (as indicators of cardiac sympathovagal balance) tended to be augmented as well in the NVC+ group. The sympathetic nerve activity to muscle response to the cold pressor test was increased in the NVC+ group versus the NVC− group (+15 ± 11 versus 6 ± 12 bursts/min; P = 0.05), but hemodynamic and sympathetic nerve responses to lower-body negative pressure did not differ between the two groups. It is concluded that NVC of the rostral ventrolateral medulla in patients with essential hypertension is accompanied by increased central sympathetic outflow. Therefore, these data support the hypothesis described in the literature: in a subgroup of patients, essential hypertension might be causally related to NVC of the rostral ventrolateral medulla, at least in part, via an increase in central sympathetic outflow.

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Stith, R. D., and K. J. Dormer. "Pressor and endocrine responses to lesions of canine rostral ventrolateral medulla." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 6 (June 1, 1994): H2520—H2526. http://dx.doi.org/10.1152/ajpheart.1994.266.6.h2520.

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To understand the mechanism(s) of reduction in arterial pressure (AP) after kainic acid cytotoxic lesions in the rostral ventrolateral medulla (RVLM), recordings of AP, cardiac output (CO), heart rate (HR), plasma catecholamines, and cortisol were obtained from awake relaxed dogs. Mongrels (n = 12) were instrumented with a solid-state pressure transducer in the descending aorta and a pulse transit-time ultrasonic flowmeter on the aortic arch. After the dogs recovered from thoracotomy, AP, CO, HR, and plasma levels of epinephrine, norepinephrine, and cortisol were recorded periodically or measured at rest over 2–3 wk followed by unilateral, cytotoxic lesion placement in the rostral C1 area of the RVLM. After the dogs recovered from lesion surgery, the measurements were repeated, and, compared with prelesion control values, they showed significantly decreased AP (-23.1 mmHg) and total peripheral resistance (-0.014 peripheral resistance units) but no significant changes in CO or HR. The reduction in AP may be caused partially by significant reductions in plasma epinephrine (-47%), norepinephrine (-34%), and cortisol (-66%) levels. Lesion sites corresponded to the rostral C1 area, immunocytochemically positive for phenylethanolamine-N-methyltransferase (PNMT). These observations support the concept that a discrete site in the RVLM, demarcated by a rostral subgroup of PNMT-immunoreactive cell bodies, contributes to direct sympathoexcitatory support of resting AP. The neurotransmitter responsible for vasomotor tone, however, remains unknown. This study also provides new information suggesting a role for catecholamine and cortisol regulation from this putative vasomotor center.

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Dampney, R. A. L., A. K. Goodchild, and R. M. McAllen. "Vasomotor control by subretrofacial neurones in the rostral ventrolateral medulla." Canadian Journal of Physiology and Pharmacology 65, no. 8 (August 1, 1987): 1572–79. http://dx.doi.org/10.1139/y87-247.

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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?

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Krassioukov, A. V., and L. C. Weaver. "Connections between the pontine reticular formation and rostral ventrolateral medulla." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (October 1, 1993): H1386—H1392. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1386.

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Pontine reticular formation (PRF) neurons provide tonic excitatory drive to sympathetic nerves and are involved in cardiovascular control [K. Hayes and L. C. Weaver. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1567-H1575, 1992]. However, connections between the PRF and the well-known vasomotor region in the rostral ventrolateral medulla (RVLM) are unknown. In propofol (Diprivan)- anesthetized rats we investigated arterial pressure, heart rate, and renal nerve responses to microinjection of glycine (1.0 M, 60 nl) into the PRF before and after injection of the synaptic blocking agent cobalt chloride (4.0 mM, 200 nl) into the RVLM. Glycine injections into the PRF caused decreases in arterial pressure, heart rate, and discharge of renal sympathetic nerves. Synaptic blockade of the RVLM almost eliminated cardiovascular and sympathetic responses to glycine injections into the PRF and blocked somatosympathetic reflexes in the renal nerve. Cobalt injections into the RVLM had very small effects on basal renal nerve firing, arterial pressure, or heart rate. These results suggest that the neurons within the RVLM relay influences from the PRF to sympathetic preganglionic neurons. Because injections of the excitatory amino acid antagonist, kynurenate, into the RVLM also interrupted responses to blockade of the PRF and blocked somatosympathetic reflexes, glutamate is a likely neurotransmitter from the PRF to the RVLM and for somatosympathetic reflexes.

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Kiely, J. M., and F. J. Gordon. "Role of rostral ventrolateral medulla in centrally mediated pressor responses." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 4 (October 1, 1994): H1549—H1556. http://dx.doi.org/10.1152/ajpheart.1994.267.4.h1549.

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The region of the rostral ventrolateral medulla (RVLM) plays an important role in central nervous system regulation of cardiovascular function. The initial purpose of these studies was to determine whether synaptic activation of excitatory amino acid (EAA) receptors in the RVLM might mediate central pressor responses. Blockade of EAA receptors in the RVLM with kynurenic acid abolished pressor responses evoked by stimulation of sciatic nerve afferents but had no effect on increases in arterial pressure produced by stimulation of hypothalamic sites. To determine whether synaptic transmission in the RVLM, independent of EAA receptor activation, was a prerequisite for the production of hypothalamic pressor responses, axonal conduction and/or synaptic transmission were pharmacologically interrupted in the RVLM. Blockade of synaptic transmission with muscimol or kainic acid attenuated, but did not eliminate, hypothalamic pressor responses. Concurrent blockade of synaptic and axonal transmission in the RVLM with lidocaine produced the greatest reduction of hypothalamic pressor responses. Collectively, these results suggest that central pressor responses are not uniformly mediated by synaptic activation of neurons within the RVLM. Instead, a combination of synaptic transmission and axonal conduction within and possibly outside the region of the RVLM may be required for the production of many centrally mediated pressor responses.

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Vasquez, E. C., S. J. Lewis, K. J. Varner, and M. J. Brody. "Chronic lesion of rostral ventrolateral medulla in spontaneously hypertensive rats." Hypertension 19, no. 2_Suppl (February 1, 1992): II154. http://dx.doi.org/10.1161/01.hyp.19.2_suppl.ii154.

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Kubo, Takao, Kyoji Taguchi, Motoaki Amano, Takanobu Ishizuka, Shuji Ozaki, Jin-Liang Yue, and Yoshimi Misu. "Centrally antihypertensive mechanisms and the rostral ventrolateral medulla vasomotor center." Japanese Journal of Pharmacology 64 (1994): 45. http://dx.doi.org/10.1016/s0021-5198(19)49909-5.

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Bergamaschi, C., RR Campos, N. Schor, and OU Lopes. "IMPORTANCE OF ROSTRAL VENTROLATERAL MEDULLA IN RATS WITH GOLDBLATT HYPERTENSION." Fundamental & Clinical Pharmacology 11, S1 (December 1997): 92s—93s. http://dx.doi.org/10.1111/j.1472-8206.1997.tb00885.x.

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Journal articles on the topic 'Rostral ventrolateral medulla'

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