LESION OF THE COMMISSURAL NUCLEUS OF THE SOLITARY TRACT/A2 NORADRENERGIC NEURONS FACILITATES THE ACTIVATION OF ANGIOTENSINERGIC MECHANISMS IN RESPONSE TO HEMORRHAGE
Nenhuma Miniatura disponível
Data
2013-12-19
Autores
Freiria-Oliveira, A. H. [UNESP]
Blanch, G. T. [UNESP]
Paula, Patricia Maria de [UNESP]
Menani, José Vanderlei [UNESP]
Colombari, Débora Simões de Almeida [UNESP]
Título da Revista
ISSN da Revista
Título de Volume
Editor
Elsevier B.V.
Resumo
In the present study, we investigated the effects of lesions of A2 neurons of the commissural nucleus of the solitary tract (cNTS) alone or combined with the blockade of angiotensinergic mechanisms on the recovery of arterial pressure (AP) to hemorrhage in conscious rats. Male Holtzman rats (280-320 g) received an injection of anti-dopamine-beta-hydroxylase-saporin (12.6 ng/60 nl; cNTS/A2lesion, n = 28) or immunoglobulin G (IgG)-saporin (12.6 ng/60 nl, sham, n = 24) into the cNTS and 15-21 days later had a stainless steel cannula implanted in the lateral ventricle. After 6 days, rats were submitted to hemorrhage (four blood withdrawals, 2 ml/300 g of body weight every 10 min). Both cNTS/A2-lesioned and sham rats had similar hypotension to hemorrhage (-62 +/- 7 and -73 +/- 7 mmHg, respectively), however cNTS/A2-lesioned rats rapidly recovered from hypotension (-5 +/- 3 mmHg at 30 min), whereas sham rats did not completely recover until the end of the recording (--20 +/- 3 mmHg at 60 min). Losartan (angiotensin type 1 receptor antagonist) injected intracerebroventricularly (100 mu g/1 mu l) or intravenously (i.v.) (10 mg/kg of body weight) impaired the recovery of AP in cNTS/A2-lesioned rats (-24 +/- 6 and -35 +/- 7 mmHg at 30 min, respectively). In sham rats, only i.v. losartan affected the recovery of AP' (-39 +/- 6 mmHg at 60 min). The results suggest that lesion of the A2 neurons in the cNTS facilitates the activation of the angiotensinergic pressor mechanisms in response to hemorrhage. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.
Descrição
Palavras-chave
angiotensin II, arterial pressure, losartan, AT1 receptors, catecholamine.
Como citar
Neuroscience. Oxford: Pergamon-elsevier Science Ltd, v. 254, p. 196-204, 2013.