(Hypertension. 1999;34:744-747.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Rostral Ventrolateral Medulla
A Source of Sympathetic Activation in Rats Subjected to Long-Term Treatment With L-NAME
From the Department of Physiology, UNIFESP, Escola Paulista de Medicina, São Paulo, Brazil.
Correspondence to Cássia T. Bergamaschi, Departamento de Fisiologia, Universidade Federal de São Paulo–Escola Paulista de Medicina, Rua Botucatu, 862, CEP 04023-060, São Paulo, SP, Brazil. E-mail cassia{at}fisiocardio.epm.br
Abstract—The major aim of the present study was to evaluate the role of the rostral ventrolateral medulla (RVLM) in the maintenance of hypertension in rats subjected to long-term treatment with NG-nitro-L-arginine methyl ester (L-NAME) (70 mg/kg orally for 1 week). We inhibited or stimulated RVLM neurons with the use of drugs such as glycine, L-glutamate, or kynurenic acid in urethane-anesthetized rats (1.2 to 1.4 g/kg IV). Bilateral microinjection of glycine (50 nmol, 100 nL) into the RVLM of hypertensive rats produced a decrease in mean arterial blood pressure (MAP) from 158±4 to 71±4 mm Hg (P<0.05), which was similar to the decrease produced by intravenous administration of hexamethonium. In normotensive rats, glycine microinjection reduced MAP from 106±4 to 60±3 mm Hg (P<0.05). Glutamate microinjection into the RVLM produced a significant increase in MAP in both hypertensive rats (from 157±3 to 201±6 mm Hg) and normotensive rats (from 105±5 to 148±9 mm Hg). No change in MAP was observed in response to kynurenic acid microinjection into the RVLM in either group. These results suggest that hypertension in response to long-term L-NAME treatment is dependent on an increase in central sympathetic drive, mediated by RVLM neurons. However, glutamatergic synapses within RVLM are probably not involved in this response.
Key Words: vasomotor system • rostral ventrolateral medulla • hypertension, experimental • L-NAME • glutamate
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