Use este identificador para citar ou linkar para este item: http://repositorio.ufc.br/handle/riufc/5725
Tipo: Artigo de Periódico
Título: Angiotensin receptor blockers for bipolar disorder
Autor(es): Queiroz, Ana Isabelle de Góis
Medeiros, Camila Dantas
Ribeiro, Bruna Mara Machado
Lucena, David Freitas de
Macêdo, Danielle Silveira
Palavras-chave: Angiotensinas;Transtorno Bipolar
Data do documento: Mar-2013
Instituição/Editor/Publicador: Medical Hypotheses
Citação: QUEIROZ, A. I. de G. et al. Angiotensin receptor blockers for bipolar disorder, v. 80, n. 3, p. 259-263, mar. 2013.
Abstract: Studies have suggested that the brain renin angiotensin system (RAS) regulates cerebral flow, autonomic and hormonal systems, stress, innate immune response and behavior, being implicated in several brain disorders such as major depression, Parkinson’s and Alzheimer’s disease. The angiotensin II receptor sub- type 1 (AT1R) is distributed in brain regions responsible for the control of stress response through periph- eral and central sympathetic hyperactivation as well as in the hypothalamic paraventricular region, areas known for the release of several neurotransmitters related to inflammatory response facilitation. This relationship leads to the assumption that AT1R might be the receptor most related to the central delete- rious actions of angiotensin II. New evidences from clinical studies have shown a possible role for RAS in the pathogenesis of bipolar disorder (BD), a multifactorial disorder with acknowledged presence of neu- ronal damage via oxidative stress in brain areas such as hippocampus, prefrontal cortex and striatum. Given the studies highlighting AT1R activation as a central pro-inflammatory pathway and, conversely, the involvement of inflammatory response in the pathogenesis of BD; this paper hypothesizes the use of AT1R antagonists for BD management and prevention of its neuroprogression, due to their anti-inflam- matory and neuroprotective effects.
URI: http://www.repositorio.ufc.br/handle/riufc/5725
ISSN: 0306-9877
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