Inflammation of some visceral sensory systems and autonomic dysfunction in cardiovascular disease.

Autor: Lataro RM; Department of Physiological Sciences, Center of Biological Sciences, Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil. Electronic address: renata.lataro@ufsc.br., Brognara F; Department of Nursing, General and Specialized, Nursing School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil., Iturriaga R; Facultad de Ciencias Biológicas, Pontificia Universidad Catolica de Chile, Santiago, Chile; Centro de Investigación en Fisiología y Medicina en Altura - FIMEDALT, Universidad de Antofagasta, Antofagasta, Chile., Paton JFR; Manaaki Manawa - The Centre for Heart Research, Department of Physiology, Faculty of Medical & Health Sciences, University of Auckland, Grafton, Auckland, New Zealand.
Jazyk: angličtina
Zdroj: Autonomic neuroscience : basic & clinical [Auton Neurosci] 2024 Feb; Vol. 251, pp. 103137. Date of Electronic Publication: 2023 Dec 07.
DOI: 10.1016/j.autneu.2023.103137
Abstrakt: The sensitization and hypertonicity of visceral afferents are highly relevant to the development and progression of cardiovascular and respiratory disease states. In this review, we described the evidence that the inflammatory process regulates visceral afferent sensitivity and tonicity, affecting the control of the cardiovascular and respiratory system. Some inflammatory mediators like nitric oxide, angiotensin II, endothelin-1, and arginine vasopressin may inhibit baroreceptor afferents and contribute to the baroreflex impairment observed in cardiovascular diseases. Cytokines may act directly on peripheral afferent terminals that transmit information to the central nervous system (CNS). TLR-4 receptors, which recognize lipopolysaccharide, were identified in the nodose and petrosal ganglion and have been implicated in disrupting the blood-brain barrier, which can potentiate the inflammatory process. For example, cytokines may cross the blood-brain barrier to access the CNS. Additionally, pro-inflammatory cytokines such as IL-1β, IL-6, TNF-α and some of their receptors have been identified in the nodose ganglion and carotid body. These pro-inflammatory cytokines also sensitize the dorsal root ganglion or are released in the nucleus of the solitary tract. In cardiovascular disease, pro-inflammatory mediators increase in the brain, heart, vessels, and plasma and may act locally or systemically to activate/sensitize afferent nervous terminals. Recent evidence demonstrated that the carotid body chemoreceptor cells might sense systemic pro-inflammatory molecules, supporting the novel proposal that the carotid body is part of the afferent pathway in the central anti-inflammatory reflexes. The exact mechanisms of how pro-inflammatory mediators affects visceral afferent signals and contribute to the pathophysiology of cardiovascular diseases awaits future research.
(Copyright © 2023 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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