Angiotensin II activates pressor and depressor sites of the pontomedulla that react to glutamate

1. In cats anaesthetized with a mixture of α-chloralose (40 mg/kg) and urethane (400 mg/kg) and in rats anaesthetized with a mixture of α-chloralose (60 mg/kg) and urethane (800 mg/kg), changes in systemic arterial pressure (SAP), heart rate (HR) and sympathetic activities of vertebral (VNA) and renal (RNA) nerves were determined following the microinjection of angiotensin II (AngII; 0.16 mmol/L; 50 nL) into the presser and depressor sites of the pontomedulla previously reacted to a microinjection of monosodium L-glutamate (Glu; 0.1 mol/L; 50 nL). Presser sites included gigantocellular tegmental field (FTG) and dorsal medulla (DM) and rostral ventrolateral medulla (VLM). The depressor site was the caudal VLM (CVLM). The effects of losartan (1 mmol/L; 50 nL), a specific AT₁ receptor non-peptide antagonist for AngII, on responses induced by AngII in the VLM, DM and CVLM were also determined. 2. In 30% of presser sites in the FTG, 55% in the VLM and 67% in the DM and in 76% of depressor sites in the CVLM previously exposed to Glu, microinjection of AngII to the same site produced presser or depressor responses similar to that of Glu, but smaller in magnitude, particularly in the presser VLM. Changes in both VNA and RNA induced by AngII were also smaller than those induced by Glu, particularly RNA from DM activation. 3. In the dorsal motor nucleus of the vagus, AngII, as Glu, produced marked bradycardia, but again this was smaller in magnitude than the bradycardia produced by Glu. 4. In rats, in the DM near or around the nucleus of the solitary tract where Glu increased SAP, microinjection of AngII (0.8 mmol/L; 60 nL) produced a depressor response, while the microinjection of 1.6 mmol/L (60 nL) AngII produced a presser response. 5. Losartan blocked the increases in SAP induced by AngII in the VLM and DM. Decreases in SAP induced by AngII in the CVLM, however, were only slightly decreased by losartan. 6. Our data suggest that a significant portion of presser and depressor sites of the pontomedulla contain neurons responsive to both AngII and Glu. In neurons in the VLM and DM, AngII produced presser responses that were primarily mediated through AT₁ receptors, while the depressor actions of AngII in the CVLM were not mediated by AT₁ receptors.