PUTATIVE PATHWAYS INVOLVED IN CARDIOVASCULAR-RESPONSES EVOKED FROM THE CAUDAL PRESSER AREA

1. The caudal presser area (CPA) is a recently identified site within the ventrolateral medulla which is involved in cardiovascular regulati on. CPA chemical stimulation by L-glutamate produces an increase in ar terial blood pressure (ABP) while its inhibition by GABA or glycine ev okes marked hypotension. In the present study, we sought to determine the potential neural pathways underlying these responses. 2. In uretha ne-anesthetized, paralyzed, artificially ventilated rats, CPA inhibiti on by bilateral microinjection of the inhibitory amino acid glycine (G ly, 100 nmol 200 nl(-1) site(-1)) produced an average decrease of -38 +/- 4.3 mmHg in ABP (N = 6). Ten min after bilateral microinjection of the broad-spectrum glutamate antagonist kynurenic acid (KYN, 2 nmol 2 00 nl(-1) site(-1)) into the caudal ventrolateral medulla (CVLM) depre ssor responses to CPA inhibition were virtually abolished (-3 +/- 1.7 mmHg, P<0.05). Similar microinjection of KYN into the rostral ventrola teral medulla (RVLM) or into the CPA itself did not modify depressor r esponses to CPA inhibition by glycine. 3. CPA stimulation by bilateral microinjection of the excitatory amino acid L-glutamate (L-glu, 50 nm ol 200 nl(-1) site(-1)) produced an increase in ABP (+43 +/- 5.4 mmHg, N = 6). Bilateral microinjection of the GABA A antagonist bicuculline methiodide (BIC, 200 pmol 200 nl(-1) site(-1)). into the CVLM markedl y reduced presser responses to CPA stimulation (+6 +/- 2.7 mmHg, P<0.0 5). similar application of BIC into the RVLM or CPA did not modify pre sser responses to CPA stimulation by glutamic acid. 4. These results d emonstrate that cardiovascular responses to CPA excitation or inhibiti on are mediated by the CVLM, and that glutamatergic and GABAergic syna pses are involved. We conclude that CPA acts by modulating the sympath oinhibitory function of the caudal ventrolateral medulla.