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Tipo do documento: Artigo
Título: Involvement of catecholaminergic medullary pathways in cardiovascular responses to acute changes in circulating volume
Autor: Cravo, Sergio Luiz Domingues
Lopes, Oswaldo Ubríaco
Pedrino, Gustavo Rodrigues
Abstract: Water deprivation and hypernatremia are major challenges for water and sodium homeostasis. Cellular integrity requires maintenance of water and sodium concentration within narrow limits. This regulation is obtained through engagement of mul- tiple mechanisms and neural pathways that regulate the volume and composition of the extracellular fluid. The purpose of this short review is to summarize the literature on central neural mechanisms underlying cardiovascular, hormonal and autonomic responses to circulating volume changes, and some of the findings obtained in the last 12 years by our laboratory. We review data on neural pathways that start with afferents in the carotid body that project to medullary relays in the nucleus tractus solitarii and caudal ventrolateral medulla, which in turn project to the median preoptic nucleus in the forebrain. We also review data sug- gesting that noradrenergic A1 cells in the caudal ventrolateral medulla represent an essential link in neural pathways controlling extracellular fluid volume and renal sodium excretion. Finally, recent data from our laboratory suggest that these structures may also be involved in the beneficial effects of intravenous infusion of hypertonic saline on recovery from hemorrhagic shock.
Palavras-chave: Baroreceptors
Blood pressure
A1 noradrenergic neurons
Hypertonic saline
Renal vascular conductance
País: Brasil
Unidade acadêmica: Instituto de Ciências Biológicas - ICB (RG)
Citação: CRAVO, S. L.; LOPES, O. U.; PEDRINO, G. R. Involvement of catecholaminergic medullary pathways in cardiovascular responses to acute changes in circulating volume. Brazilian Journal of Medical and Biological Research, Ribeirão Preto, v. 44, n. 9, p. 877-882, Sept. 2011.
Tipo de acesso: Acesso Aberto
Identificador do documento: 10.1590/S0100-879X2011007500092 
Identificador do documento: 10.1590/S0100-879X2011007500092 
Data de publicação: Set-2011
Aparece nas coleções:ICB - Artigos publicados em periódicos

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