Please use this identifier to cite or link to this item: http://www.repositorio.ufop.br/handle/123456789/1807
Title: Malnutrition enhances cardiovascular responses to chemoreflex activation in awake rats.
Authors: Penitente, Arlete Rita
Fernandes, Luciano Gonçalves
Cardoso, Leonardo Máximo
Silva, Marcelo Eustáquio
Pedrosa, Maria Lúcia
Silva, Antônio Leite
Haibara, Andréa Siqueira
Moraes, Márcio Flávio Dutra
Chianca Júnior, Deoclécio Alves
Keywords: Albumin
Low-protein diet
Sympathetic activity
Arterial pressure
Chemoreflex
Issue Date: 2007
Citation: PENITENTE, A. R. et al. Malnutrition enhances cardiovascular responses to chemoreflex activation in awake rats. Life Sciences, v. 81, n. 7, p. 609-614, jul. 2007. Disponível em: <https://www.sciencedirect.com/science/article/pii/S0024320507005085>. Acesso em: 26 nov. 2012.
Abstract: Several studies in the literature suggest that low-protein intake is associated with increases in sympathetic efferent activity and cardiovascular disease. Among the possible mechanisms, changes in the neurotransmission of cardiovascular reflexes have been implicated. Therefore, the present study comprised the evaluation of chemoreflex responsiveness in rats subjected to a low-protein diet during the 35 days after weaning. As a result, we observed that malnourished rats presented higher levels of baseline mean arterial pressure and heart rate and exhibited a mild increase in the pressor response to chemoreflex activation. They also exhibited a massive bradycardic response to chemoreflex activation. Interestingly, bilateral ligature of the carotid body arteries further increased baseline mean arterial pressure and heart rate in malnourished animals. The data suggest severe autonomic imbalance and/or change in the central interplay between neural and cardiovascular mechanisms.
URI: http://www.repositorio.ufop.br/handle/123456789/1807
ISSN: 00243205
metadata.dc.rights.license: O periódico Life Sciences concede permissão para depósito deste artigo no Repositório Institucional da UFOP. Número da licença: 3314370163366.
Appears in Collections:DECBI - Artigos publicados em periódicos

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