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Control of the Upper Airway during Sleep
Published in Susmita Chowdhuri, M Safwan Badr, James A Rowley, Control of Breathing during Sleep, 2022
The adrenergic neurons located in the rostral ventrolateral medulla (C1 group) are important for the regulation of sympathetic tone, especially under the hypoxic and hypercapnic conditions and under stress (170–172). To date, little is known about any contribution of these cells to the regulation of cardiorespiratory changes with sleep-wake states, but recent data indicate that at least the caudal cohort of C1 cells is activated during pharmacologically induced REM sleep-like state (173), and activation of these cells is associated with the termination of non-REM sleep (174).
Regulation of Arterial Blood Pressure
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Rostral ventrolateral medulla (RVLM). This group of neurons (vasomotor area) is a major source of excitatory input to sympathetic nerves controlling the peripheral blood vessels. The RVLM neurons are tonically active and send information via axons that run dorsally and medially and then descend in the lateral column of the spinal cord to the thoracolumbar intermediolateral grey column. This results in an increase in cardiac output and peripheral vascular resistance. The neurotransmitter is glutamate. The tonic activity is inhibited by the baroreceptor reflex.
Organization of Central Respiratory Neurons
Published in Alan D. Miller, Armand L. Bianchi, Beverly P. Bishop, Neural Control of the Respiratory Muscles, 2019
Armand L. Bianchi, Rosario Pásaro
In addition to the NPGL, the retrotrapezoid nucleus (RTN), which represents a cluster of neurons adjacent to the ventral surface of the rostral medulla at the level of the retrofacial and facial nuclei, also projects to the DRG and VRG.69 It has been suggested that the RTN and NPGL provide the neural substrate mediating the effects of stimulation of the ventral surface of the brainstem following changes in the chemical environment of neurons controlling respiration and circulation. Neurons in the rostral ventrolateral medulla are also involved in cardiovascular regulation, but their functional relations with RTN neurons are unclear.
Novel approaches: targeting sympathetic outflow in the carotid sinus
Published in Blood Pressure, 2023
Dagmara Hering, Krzysztof Narkiewicz
Tonic sympathetic activation and tonic arterial BP control depend on central integrative structures in the brain stem, the rostral ventrolateral medulla (RVLM) [3]. Descending projections to the RVLM arise among others from the neurons in the peri-aqueductal grey and hypothalamic paraventricular nucleus (PVN). The RVLM integrates reflex neural mechanisms from arterial baroreceptors, chemoreceptors and various afferent sensory visceral receptors via direct connection with the upper part of the medulla through the NTS and PVN which modulate vasomotor sympathetic nerve discharge and BP. Under physiological conditions, arterial baroreceptors play a fundamental role in preventing excessive variability in BP. Afferent signals from baroreceptors stimulate the NTS in the upper part of the medulla in response to the distension of the vessel wall caused by transmural pressure. A signal arising from the NTS exerts a parasympathetic vagal effect resulting in slowing HR and reducing tonic sympathetic activity generated in the RVLM (Figure 2).
Overexpression of NaV1.6 in the rostral ventrolateral medulla in rats mediates stress-induced hypertension via glutamate regulation
Published in Clinical and Experimental Hypertension, 2022
Lei Tong, Mengyu Xing, Jiaxiang Wu, Shuai Zhang, Dechang Chu, Haili Zhang, Fuxue Chen, Dongshu Du
Stress-induced hypertension (SIH) caused by central sympathetic nerve disorder is the main type of primary hypertension induced by aggravated social and psychological stress among adults (1). Stress can activate a series of pathological molecular and cellular alterations, leading to induction of cardiovascular disease via the central nervous system (2). For instance, neuron activity and sympathetic overactivity in the rostral ventrolateral medulla (RVLM) are involved in the regulation of hypertension (3). Several studies have demonstrated that the RVLM is responsible for generating the sympathetic drive to the cardiovascular system and eventually determines cardiac output and vascular resistance (4). Recent studies of the signaling axis of the central nervous system, which regulates blood pressure, have found that changes in sodium, potassium, and calcium plasma channels in specific brain regions are related to the regulation of hypertension (5). Our previous studies also found that overexpression of NaV1.6 in the RVLM and increased KV10.2 expression in the paraventricular nucleus after stress are related to increased blood pressure (6,7).
«A case of a pharmacoresistant tachyarrhythmia associated with Arnold-Chiari malformation»
Published in British Journal of Neurosurgery, 2019
I. M. Gilemkhanova, Shamil Safin, Khristina Derevyanko, Albert Gilemkhanov, Igor Buzaev
Indeed, a transient malfunction at the brain stem level could affect several structures involved in sympathetic/parasympathetic cardiovascular regulation constituting the baroreflex system. The baroreflex system is mediated by afferent pathways via the ninth and tenth cranial nerves, relaying information from vascular baroreceptors to the nucleus tractus solitarii (NTS), which sends excitatory projections to the caudal ventrolateral medulla, which in turn inhibits the sympathoexcitatory neurones of the rostral ventrolateral medulla. Lesions of the NTS or efferent/afferent baroreflex pathways result in baroreflex failure, leading typically to a marked lability of blood pressure, with hypertension and tachycardia alternating with hypotension and bradycardia. However, depending on the degree and probably the site of injury of the baroreflex mediating system, other clinical presentations could occur, such as tachycardia.8,10–12