Please use this identifier to cite or link to this item: http://www.repositorio.ufop.br/handle/123456789/4272
Title: Nitric oxide at the CVLM is involved in the attenuation of the reflex bradycardia in renovascular hypertensive rats.
Authors: Castro, Uberdan Guilherme Mendes de
Souza, Graziele Galdino de
Machado, Raquel do Pilar
Isoldi, Mauro César
Silva, Marcelo Eustáquio
Nadu, Ana Paula
Souza, Luiz Eduardo de
Santos, Robson Augusto Souza dos
Santos, Maria José Campagnole dos
Alzamora, Andréia Carvalho
Keywords: Caudal ventrolateral medulla
Reflex bradycardia
Nitric oxide
Superoxide anion
Renovascular hypertension-Goldblatt-2K1C
Issue Date: 2012
Citation: CASTRO, U. G. M. et al. Nitric oxide at the CVLM is involved in the attenuation of the reflex bradycardia in renovascular hypertensive rats. Nitric Oxide, v. 26, p. 118-125, 2012. Disponível em: <http://www.sciencedirect.com/science/article/pii/S1089860312000134>. Acesso em: 08 nov. 2014.
Abstract: Hypertension is associated to an increase in central oxidative stress and an attenuation of the baroreflex control of arterial pressure. The present study evaluated the effect of alterations in the levels of nitric oxide (NO) and superoxide anion in the caudal ventrolateral medulla (CVLM), a key area of the brainstem for the baroreflex control of arterial pressure, in renovascular hypertensive rats (2K1C). Baseline mean arterial pressure (MAP), heart rate (HR), and reflex bradycardia were evaluated 30 days after renal artery occlusion in anesthetized (urethane, 1.2 g/kg, i.p.) 2K1C or normotensive (SHAM) rats. The MAP, HR, and baroreflex control of HR were evaluated before and after CVLM microinjections of the non-selective NOS inhibitor L-NAME (10 nmol), the NO precursor L-ARG (50 nmol), or the antioxidant ascorbic acid, Vit C (10 nmol). In both 2K1C and SHAM animals, CVLM microinjection of L-NAME produced a decrease in MAP, whereas L-ARG induced a significant increase in MAP. However, microinjection of Vit C into the CVLM produced a decrease in MAP and HR only in 2K1C and not in SHAM rats. Cardiovascular effects produced by microinjection of L-ARG into the CVLM were abolished by prior microinjection of L-NAME in the CVLM of 2K1C and SHAM rats. Microinjection of L-NAME into the CVLM increased the sensitivity of reflex bradycardia in 2K1C animals. In contrast, the CVLM microinjection of L-ARG reduced reflex bradycardia only in SHAM rats. Vit C in the CVLM did not change reflex bradycardia in either 2K1C or in SHAM rats. These results suggest that increased oxidative stress in the CVLM during hypertension contributes to the reduced baroreflex sensitivity and to maintain hypertension in the 2K1C model.
URI: http://www.repositorio.ufop.br/handle/123456789/4272
metadata.dc.identifier.doi: https://doi.org/10.1016/j.niox.2012.01.002
ISSN: 1089-8603
metadata.dc.rights.license: O periódico Nitric Oxide concede permissão para depósito deste artigo no Repositório Institucional da UFOP. Número da licença: 3520370957775.
Appears in Collections:DECBI - Artigos publicados em periódicos

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