Inhibitory Vasomotor Neurons in the Caudal Ventrolateral Medulla Oblongata

Physiology ◽  
1991 ◽  
Vol 6 (3) ◽  
pp. 139-141 ◽  
Author(s):  
WW Blessing
Keyword(s):  
Medulla Oblongata ◽  
Gabaergic Neurons ◽  
Ventrolateral Medulla ◽  
Vasomotor Tone ◽  
Caudal Ventrolateral Medulla ◽  
Premotor Neurons ◽  
Sympathetic Vasomotor Tone

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.

scholarly journals Control of sympathetic vasomotor tone by catecholaminergic C1 neurones of the rostral ventrolateral medulla oblongata

2011 ◽  
Vol 91 (4) ◽  
pp. 703-710 ◽  
Author(s):  
N. Marina ◽  
A. P. L. Abdala ◽  
A. Korsak ◽  
A. E. Simms ◽  
A. M. Allen ◽  
...  
Keyword(s):  
Medulla Oblongata ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Vasomotor Tone ◽  
Sympathetic Vasomotor Tone

scholarly journals Glutamatergic inputs to the CVLM independent of the NTS promote tonic inhibition of sympathetic vasomotor tone in rats

2008 ◽  
Vol 295 (4) ◽  
pp. H1772-H1779 ◽  
Author(s):  
Daniel A. Mandel ◽  
Ann M. Schreihofer
Keyword(s):  
Sympathetic Nerve Activity ◽  
Nucleus Tractus Solitarius ◽  
Excitatory Input ◽  
Gabaergic Neurons ◽  
Tonic Inhibition ◽  
Ventrolateral Medulla ◽  
Respiratory Drive ◽  
Vasomotor Tone ◽  
Nerve Activity ◽  
Sympathetic Vasomotor Tone

GABAergic neurons in the caudal ventrolateral medulla (CVLM) are driven by baroreceptor inputs relayed via the nucleus tractus solitarius (NTS), and they inhibit neurons in rostral ventrolateral medulla to reduce sympathetic nerve activity (SNA) and arterial pressure (AP). After arterial baroreceptor denervation or lesions of the NTS, inhibition of the CVLM continues to increase AP, suggesting additional inputs also tonically activate the CVLM. This study examined whether the NTS contributes to baroreceptor-independent drive to the CVLM and whether glutamate promotes baroreceptor- and NTS-independent activation of the CVLM to tonically reduce SNA. In addition, we evaluated whether altering central respiratory drive, a baroreceptor-independent regulator of CVLM neurons, influences glutamatergic inputs to the CVLM. Splanchnic SNA and AP were measured in chloralose-anesthetized, ventilated, paralyzed rats. The infusion of nitroprusside decreased AP below threshold for baroreceptor afferent firing (<50 mmHg) and increased SNA to 209 ± 22% ( P < 0.05), but the subsequent inhibition of the NTS by microinjection of the GABAA agonist muscimol did not further increase SNA. In contrast, after inhibition of the NTS, blockade of glutamatergic inputs to CVLM by microinjection of kynurenate increased SNA (274 ± 54%; P < 0.05; n = 7). In vagotomized rats with baroreceptors unloaded, inhibition of glutamatergic inputs to CVLM evoked a larger rise in SNA when central respiratory drive was increased (219 ± 16% vs. 271 ± 17%; n = 5; P < 0.05). These data suggest that baroreceptor inputs provide the major drive for the NTS-mediated excitation of the CVLM. Furthermore, glutamate tonically activates the CVLM to reduce SNA independent of the NTS, and this excitatory input appears to be affected by the strength of central respiratory drive.

scholarly journals Role of the medulla oblongata in normal and high arterial blood pressure regulation: the contribution of Escola Paulista de Medicina - UNIFESP

2009 ◽  
Vol 81 (3) ◽  
pp. 589-603 ◽  
Author(s):  
Sergio L. Cravo ◽  
Ruy R. Campos ◽  
Eduardo Colombari ◽  
Mônica A. Sato ◽  
Cássia M. Bergamaschi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Medulla Oblongata ◽  
Neural Circuits ◽  
Ventrolateral Medulla ◽  
Vasomotor Tone ◽  
Arterial Blood ◽  
Pathological Conditions ◽  
De Medicina

Several forms of experimental evidence gathered in the last 37 years have unequivocally established that the medulla oblongata harbors the main neural circuits responsible for generating the vasomotor tone and regulating arterial blood pressure. Our current understanding of this circuitry derives mainly from the studies of Pedro Guertzenstein, a former student who became Professor of Physiology at UNIFESP later, and his colleagues. In this review, we have summarized the main findings as well as our collaboration to a further understanding of the ventrolateral medulla and the control of arterial blood pressure under normal and pathological conditions.

Central Neurotransmitter Pathways for Baroreceptor-Initiated Secretion of Vasopressin

Physiology ◽  
1986 ◽  
Vol 1 (3) ◽  
pp. 90-91 ◽  
Author(s):  
WW Blessing
Keyword(s):  
Neuropeptide Y ◽  
Medulla Oblongata ◽  
Neuroendocrine Cells ◽  
Ventrolateral Medulla ◽  
Caudal Ventrolateral Medulla ◽  
Functional Integrity

Secretion of vasopressin in response to hemorrhage depends on the functional integrity of noradrenaline- and neuropeptide Y-containing neurons. The effects of microinjections of neuropharmacological agents have clarified the role of these neurons, which project directly from the caudal ventrolateral medulla oblongata to the neuroendocrine cells in the hypothalamus.

Contribution to sympathetic vasomotor tone of tonic glutamatergic inputs to neurons in the RVLM

2004 ◽  
Vol 287 (6) ◽  
pp. R1335-R1343 ◽  
Author(s):  
Jouji Horiuchi ◽  
Suzanne Killinger ◽  
Roger A. L. Dampney
Keyword(s):  
Excitatory Amino Acid ◽  
Ventrolateral Medulla ◽  
Tonic Activity ◽  
Vasomotor Tone ◽  
Renal Sympathetic Nerve Activity ◽  
Vehicle Injection ◽  
Sympathetic Vasomotor Tone ◽  
Modest Reduction ◽  
Renal Sympathetic

The role of excitatory amino acid (EAA) receptors in the rostral ventrolateral medulla (RVLM) in maintaining resting sympathetic vasomotor tone remains unclear. It has been proposed that EAA receptors in the RVLM mediate excitatory inputs both to presympathetic neurons and to interneurons in the caudal ventrolateral medulla (CVLM), which then provide a counterbalancing inhibition of RVLM presympathetic neurons. In this study, we tested this hypothesis by determining the effect of blockade of EAA receptors in the RVLM on mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA), after inhibition of CVLM neurons. In anesthetized rats, bilateral injections of muscimol in the CVLM increased MAP, HR, and RSNA. Subsequent bilateral injections of kynurenic acid (Kyn, 2.7 nmol) in the RVLM caused a modest reduction of ∼20 mmHg in the MAP but had no effect, when compared with the effect of vehicle injection alone, on HR or RSNA. By ∼50 min after the injections of Kyn or vehicle in the RVLM, the MAP had stabilized at a level close to its original baseline level, but the HR and RSNA stabilized at levels above baseline. The results indicate that removal of tonic EAA drive to RVLM neurons has little effect on the tonic activity of RVLM presympathetic neurons, even when inputs from the CVLM are blocked. Thus the tonic activity of RVLM presympathetic neurons under these conditions is dependent on excitatory synaptic inputs mediated by non-EAA receptors and/or the autoactivity of these neurons.

Brain stem oxidative stress and its associated signaling in the regulation of sympathetic vasomotor tone

2012 ◽  
Vol 113 (12) ◽  
pp. 1921-1928 ◽  
Author(s):  
Samuel H. H. Chan ◽  
Julie Y. H. Chan
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Brain Stem ◽  
Ventrolateral Medulla ◽  
Future Research ◽  
Vasomotor Tone ◽  
Cellular Mechanisms ◽  
Neurogenic Hypertension ◽  
The Impact ◽  
Sympathetic Vasomotor Tone

There is now compelling evidence from studies in humans and animals that overexcitation of the sympathetic nervous system plays an important role in the pathogenesis of cardiovascular diseases. An excellent example is neurogenic hypertension, in which central sympathetic overactivation is involved in the development, staging, and progression of the disease, and one of the underlying mechanisms involves oxidative stress in key brain stem sites that are engaged in the regulation of sympathetic vasomotor tone. Using the rostral ventrolateral medulla (RVLM) and nucleus tractus solitarii (NTS) as two illustrative brain stem neural substrates, this article provides an overview of the impact of reactive oxygen species and antioxidants on RVLM and NTS in the pathogenesis of neurogenic hypertension. This is followed by a discussion of the redox-sensitive signaling pathways, including several kinases, ion channels, and transcription factors that underpin the augmentation in sympathetic vasomotor tone. In addition, the emerging view that brain stem oxidative stress is also causally related to a reduction in sympathetic vasomotor tone and hypotension during brain stem death, methamphetamine intoxication, and temporal lobe status epilepticus will be presented, along with the causal contribution of the oxidant peroxynitrite formed by a reaction between nitric oxide synthase II (NOS II)-derived nitric oxide and superoxide. Also discussed as a reasonable future research direction is dissection of the cellular mechanisms and signaling cascades that may underlie the contributory role of nitric oxide generated by different NOS isoforms in the differential effects of oxidative stress in the RVLM or NTS on sympathetic vasomotor tone.

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