Commissural NTS lesions and cardiovascular responses in aortic baroreceptor-denervated rats
Both acute (1 day) lesions of the commissural nucleus of the solitary tract (commNTS) and aortic baroreceptor denervation increase presser responses to bilateral common carotid occlusion (BCO) during a 60-second period in conscious rats. In this study, we investigated the following: (1) the effects...
| Autores: | , , , |
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| Formato: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 1999 |
| País: | Brasil |
| Recursos: | Universidade Federal de São Paulo (UNIFESP) |
| Repositorio: | Repositório Institucional da UNIFESP |
| Idioma: | inglés |
| OAI Identifier: | oai:repositorio.unifesp.br:11600/43882 |
| Acesso em linha: | https://doi.org/10.1161/01.HYP.34.4.739 http://repositorio.unifesp.br/handle/11600/43882 |
| Access Level: | acceso abierto |
| Palavra-chave: | blood pressure baroreceptors chemoreceptors solitary nucleus occlusion |
| Resumo: | Both acute (1 day) lesions of the commissural nucleus of the solitary tract (commNTS) and aortic baroreceptor denervation increase presser responses to bilateral common carotid occlusion (BCO) during a 60-second period in conscious rats. In this study, we investigated the following: (1) the effects of commNTS lesions on basal mean arterial pressure (MAP) and heart rate (HR) of aortic denervated (ADNx) rats; (2) the effects of acute commNTS lesions on presser responses to BCO in ADNx rats; and (3) the effects of chronic (10 days) commNTS lesions on the presser response to BCO, ADNx increased basal MAP and HR in sham-lesioned rats. Acute commNTS lesions abolished the MAP and HR increases observed in ADNx rats. Acute commNTS lesions increased the presser responses to BCO in rats with intact-baroreceptor innervation but produced no additional change in the presser response to BCO in ADNx rats. Chronic commNTS lesions did not change the presser responses to BCO in rats with intact-baroreceptor innervation. The data shaw that acute commNTS lesions abolish the MAP increase produced by aortic baroreceptor denervation. They also suggest that acute commNTS lesions enhance the presser response to BCO by partial withdrawal of aortic baroreceptor inputs into the NTS. Chronically, reorganization in the remaining aortic baroreceptor or in the baroreflex function as a whole might produce normalization of the cardiovascular responses to BCO. |
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