INVOLVEMENT OF SPINALLY RELEASED GABA IN THE REGULATION OF BLOOD PRESSURE

CELUCH SM

Mar del Plata

Congreso; SAIC-SAI-SAFE 2016; 2016

SAIC-SAI-SAFE

INVOLVEMENT OF SPINALLY RELEASED GABA IN THE REGULATION OF BLOODPRESSURE  Celuch SM; ININFA (CONICET-UBA); Junín 956 5°P, (1113),C.A.B.A. Email: sceluch@ffyb.uba.arElectrophysiological studies showedthat the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) decreasesthe excitability of sympathetic preganglionic neurons (SPN). The inhibitoryaction of GABA at SPN was also examined by the observation of thecardiovascular effects of intrathecally (i.t.) administered agonists andantagonists for GABA receptors. Since there is little information about the roleof GABA in the effects of other neurotransmitters that regulate the bloodpressure at the level of the spinal cord,  the aim of this study was to analyze theparticipation of GABA in the hypotensive effects of i.t. administered adrenaline(ADRE, 30 nmol) and apomorphine (APO, 50 nmol) in pentobarbital-anesthetized maleSprague-Dowley rats. The hypotensive response to ADRE (-18.2±3.1mmHg, n=8) was prevented by both the GABAA-receptor antagonist bicuculline (BIC5 nmol, it; n=4) and the GABA synthesis inhibitor 3-mercaptopropionic acid(MPA, 60 mg/kg, i.p.; n=6). On the other hand, the GABA uptake inhibitor nipecoticacid (NIP, 2.3 µmol, i.t.; n=5) enhanced the effect of ADRE. Similarly to ADRE,the hypotensive response to APO (-16.0 + 2.8 mmHg; n=7) was abolished by MPA and BIC (n=5), although it wasunmodified by NIP (n=6). The response to APO was instead increased by diazepam(105 nmol, it; n=4), a drug that potentiate the effects of GABA by binding tothe allosteric benzodiazepine site at GABAA-receptor. Diazepam did not modify thehypotensive effect of ADRE. It is suggested that the hypotensive effects caused byneurotransmitters/neuromodulators such as catecholamines and dopamine at the spinalcord involve the release of GABA at the surroundings of SPN. Supported byCONICET (PIP 201201-00425).