Please use this identifier to cite or link to this item: http://repositorio.unifesp.br/handle/11600/28513
Title: Attenuated pressor responses to amino acids in the rostral ventrolateral medulla after swimming training in conscious rats
Authors: Martins-Pinge, M. C.
Becker, L. K.
Garcia, MRL
Zoccal, D. B.
Neto, R. V.
Basso, L. S.
Souza, HCD de
Lopes, O. U.
Universidade Estadual de Londrina (UEL)
Universidade Federal de São Paulo (UNIFESP)
Keywords: blood pressure
exercise training
sympathetic nervous system
glutamate receptors
Issue Date: 30-Oct-2005
Publisher: Elsevier B.V.
Citation: Autonomic Neuroscience-basic & Clinical. Amsterdam: Elsevier B.V., v. 122, n. 1-2, p. 21-28, 2005.
Abstract: The cardiovascular effects of microinjection of the amino acids glutamate and glycine within the rostral ventrolateral medulla (RVLM) after swimming training (ST) in unrestrained awake rats were investigated. Unilateral microinjection of L-glutamate (5, 20 and 50 MM, in 100 nl) produced a dose dependent increase in mean arterial pressure (MAP) in control (C) (16 +/- 5 mm Hg; 29 +/- 6 min Hg; 43 +/- 6 mm Hg) and swim (SW) (1 +/- 1 mm Hg; 16 2 mm Hg; 25 3 min Hg) groups. However, the magnitude of this response was lower in the swim group. Prazosin injection produced hypotension and tachycardia in both groups (C = -43 +/- 3 mm Hg/98 +/- 16 bpm; SW = -61 +/- 5 mm Hg/115 +/- 32 bpm). in the SW group the hypotension caused by prazosin was greater compared to C group, but the tachycardia was not different between them. After prazosin, glutamate response in RVLM was blocked in both groups as well. When glycine (10 mM or 1 M, in 100 nl) were microinjected into the RVLM of C group we observed two different effects: decrease in MAP with the lower dose and an increase in MAP with the higher dose (10 mM = -13 +/- 2 mm Hg; 1 M = 47 +/- 6 mm Hg). However, after ST the hypertensive response to glycine was blunted with no alterations in the hypotensive response (10 mM = -14 +/- 1 mm Hg; 1 M = 18 +/- 4 mm Hg). These findings suggest that RVLM is involved in the modulation of the sympathetic outflow to the cardiovascular system during exercise training. (c) 2005 Elsevier B.V. All rights reserved.
URI: http://repositorio.unifesp.br/handle/11600/28513
ISSN: 1566-0702
Other Identifiers: http://dx.doi.org/10.1016/j.autneu.2005.07.007
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