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Evidence of an endogenous forebrain GABAergic system capable of inhibiting baroreceptor-mediated vasopressin release

1989; Elsevier BV; Volume: 499; Issue: 1 Linguagem: Inglês

10.1016/0006-8993(89)91134-7

1872-6240

Ted Segura, Eileen M. Hasser, Robert E. Shade, Joseph R. Haywood,

Photoreceptor and optogenetics research

In conscious rats, intracerebroventricular (i.c.v.) injections of γ-aminobutyric acid (GABA), a GABA-uptake inhibitor (nipecotic acid), and artificial CSF (aCSF) were restricted to forebrain regions and their effect on baroreceptor-mediated arginine-vasopressin (AVP) release was studied. AVP release was stimulated by the hypotension resulting from combined treatment with a converting enzyme inhibitor (CEI) and chlorisondamine (CHLOR), a ganglionic blocking agent.CEI+CHLOR reduced mean arterial pressure (MAP) from118±2to63±2mm Hg, but pressure then rose to a compensated level of78±1mm Hg. The compensation in MAP was shown to be AVP-dependent at the end of the experiment since the vascular AVP antagonist, d(CH2)5Tyr(Me)AVP, reduced MAP from78±1to63±1mm Hg. While AVP was contributing to MAP maintenance, GABA (15, 50 and 150 μg) caused dose-related reductions in MAP (5±1,7±1and11±2mm Hg, respectively). Nipecotic acid (3–350 μg) also caused dose-related reductions in MAP (from3±1to15±2mm Hg), while aCSF had no effect on MAP. Pretreatment with d(CH2)5Tyr(Me)AVP, antagonized completely the depressor effects of GABA and nipecotic acid. In other rats, blood samples were taken to measure the changes in plasma AVP concentrations (pAVP) induced byCEI+CHLOR and subsequent treatment with aCSF or nipecotic acid (175 μg). Hypotension induced byCEI+CHLOR caused a significant increase in pAVP. Forebrain-restricted nipecotic acid significantly suppressed pAVP (61 ± 8%reduction; P < 0.05vs aCSF). These data provide evidence of an endogenous forebrain GABAergic system which, when activated, can inhibit baroreceptor-mediated AVP release.