Inhibition of neurons in commissural nucleus of solitary tract reduces sympathetic nerve activity in SHR

Inhibition of neurons in commissural nucleus of solitary tract reduces sympathetic nerve activity in SHR

Autor Sato, Monica A. Autor UNIFESP Google Scholar
Colombari, Eduardo Autor UNIFESP Google Scholar
Morrison, Shaun F. Google Scholar
Instituição Northwestern Univ
Universidade Federal de São Paulo (UNIFESP)
Resumo Neurons in the commissural nucleus of the solitary tract (commNTS) play an important role in certain cardiovascular responses dependent on sympathetic vasoconstrictor activation, including the arterial chemoreceptor reflex. Electrolytic lesions of the commNTS elicit a fall in arterial pressure (AP) in spontaneously hypertensive rats (SHR). To determine whether the latter result 1) arose from elimination of commNTS neuronal activity rather than en passant axons and 2) was accompanied by a reduction in sympathetic nerve activity, we evaluated the effect of inhibition of neurons in the commNTS on basal splanchnic sympathetic nerve activity (SNA), AP, and heart rate (HR) in SHR, Wistar-Kyoto (WKY), and Sprague-Dawley (SD) rats. in chloralose-anesthetized, paralyzed, and artificially ventilated SHR, microinjection of GABA into the commNTS markedly decreased splanchnic SNA, AP, and HR. the reductions in SNA and AP following similar microinjections in WKY and SD rats were significantly less than those in SHR. Our findings suggest that tonically active neurons in the commNTS contribute to the maintenance of SNA and the hypertension in SHR. the level of tonic discharge of these commNTS neurons in normotensive WKY and SD rats may be lower than in SHR.
Assunto sympathetic nerve activity
spontaneously hypertensive rats
gamma-aminobutyric acid
chemoreceptor reflex
Idioma Inglês
Data 2002-05-01
Publicado em American Journal of Physiology-heart and Circulatory Physiology. Bethesda: Amer Physiological Soc, v. 282, n. 5, p. H1679-H1684, 2002.
ISSN 0363-6135 (Sherpa/Romeo, fator de impacto)
Editor Amer Physiological Soc
Extensão H1679-H1684
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000175011700014

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