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|Title:||PUTATIVE PATHWAYS INVOLVED IN CARDIOVASCULAR-RESPONSES EVOKED FROM THE CAUDAL PRESSER AREA|
|Authors:||Campos, Ruy Ribeiro [UNIFESP]|
Possas, O. S.
Cravo, Sergio Luiz [UNIFESP]
Lopes, Oswaldo Ubriaco [UNIFESP]
Guertzenstein, Pedro Gaspar [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
ARTERIAL BLOOD PRESSURE
|Publisher:||Assoc Bras Divulg Cientifica|
|Citation:||Brazilian Journal Of Medical And Biological Research. Sao Paulo: Assoc Bras Divulg Cientifica, v. 27, n. 10, p. 2467-2479, 1994.|
|Abstract:||1. The caudal presser area (CPA) is a recently identified site within the ventrolateral medulla which is involved in cardiovascular regulation. CPA chemical stimulation by L-glutamate produces an increase in arterial blood pressure (ABP) while its inhibition by GABA or glycine evokes marked hypotension. In the present study, we sought to determine the potential neural pathways underlying these responses.2. In urethane-anesthetized, paralyzed, artificially ventilated rats, CPA inhibition by bilateral microinjection of the inhibitory amino acid glycine (Gly, 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 200 nl(-1) site(-1)) into the caudal ventrolateral medulla (CVLM) depressor responses to CPA inhibition were virtually abolished (-3 +/- 1.7 mmHg, P<0.05). Similar microinjection of KYN into the rostral ventrolateral medulla (RVLM) or into the CPA itself did not modify depressor responses to CPA inhibition by glycine.3. CPA stimulation by bilateral microinjection of the excitatory amino acid L-glutamate (L-glu, 50 nmol 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 markedly reduced presser responses to CPA stimulation (+6 +/- 2.7 mmHg, P<0.05). similar application of BIC into the RVLM or CPA did not modify presser responses to CPA stimulation by glutamic acid.4. These results demonstrate that cardiovascular responses to CPA excitation or inhibition are mediated by the CVLM, and that glutamatergic and GABAergic synapses are involved. We conclude that CPA acts by modulating the sympathoinhibitory function of the caudal ventrolateral medulla.|
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