Rostral ventrolateral medulla - A source of sympathetic activation in ratssubjected to long-term treatment with L-NAME

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 sub jected to long-term treatment with N-G-nitro-L-arginine methyl ester (L-NAM E) (70 mg/kg orally for 1 week). We inhibited or stimulated RVLM neurons wi th the use of drugs such as glycine, L-glutamate, or kynurenic acid in uret hane-anesthetized rats (1.2 to 1.4 g/kg: IV). Bilateral microinjection of g lycine (50 nmol. 100 nL) into the RVLM of hypertensive rats produced a decr ease 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 administra tion of hexamethonium. In normotensive rats, glycine microinjection reduced MAP from 106+/-4 to 60+/-3 mm Hg (P<0.05). Glutamate microinjection into t he RVLM produced a significant increase in MAP in both hypertensive rats (f rom 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 micro injection into the RVLM in either group. These results suggest that hyperte nsion in response to long-term L-NAME treatment is dependent on an increase in central sympathetic drive, mediated by RVLM neurons. However, glutamate rgic synapses within RVLM are probably not involved in this response.