Activation of noradrenergic mechanism attenuates glutamate-induced vasopressor responses in the pons and medulla of cats in vivo

1. Using anesthetized cats, the authors examined the noradrenergic modulati on of the glutamate induced presser and depressor responses in various brai nstem areas, including pontine gigantocellular tegmental field (FTG), dorso medial medulla (DM), rostral ventrolateral medulla (RVLM), and caudal ventr olateral medulla (CVLM). 2. Unilateral microinjection of L-glutamate (Glu, 3 nmol in 30 nL saline) i nto FTG, DM and RVLM produced an increase in systemic arterial pressure (SA P) and a decrease in heart rate (HR), while into CVLM produced decreases of SAP and HR. 3. Application of norepinephrine (NE) into the presser areas (0.05 to 5 nmo l) did not alter the resting SAP and HR, but significantly attenuated the G lu-induced presser response with an order of potency: FTG > DM > RVLM. In t he depressor CVLM, NE alone produced a dose-dependent decrease of resting S AP and WR, but did not affect the Glu-induced depressor responses. 4. The involvement of different adrenoceptor subtypes was further investiga ted by application of selective adrenoceptor agonists including phenylephri ne (alpha1), clonidine (alpha2), and isoproterenol (beta) Responses to thes e agonists are similar to those elicited by NE, except that only alpha -adr enoceptor agonists could antagonize the Glu-induced presser responses of th e RVLM. 5. Our observations indicate that NE not only inhibits the presser mechanis ms in various brainstem areas but also elicits a direct depressor response in CVLM. These findings also suggest that NE acts more likely a neurotransm itter, rather than a modulator, in the CVLM.