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

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

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

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) from 118±2 to 63±2 mm Hg, but pressure then rose to a compensated level of 78±1 mm 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 from 78±1 to 63±1 mm Hg. While AVP was contributing to MAP maintenance, GABA (15, 50 and 150 μg) caused dose-related reductions in MAP (5±1,7±1 and 11±2 mm Hg, respectively). Nipecotic acid (3-350 μg) also caused dose-related reductions in MAP (from 3±1 to 15±2 mm 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 by CEI + CHLOR and subsequent treatment with aCSF or nipecotic acid (175 μg). Hypotension induced by CEI + CHLOR caused a significant increase in pAVP. Forebrain-restricted nipecotic acid significantly suppressed pAVP (61 ± 8% reduction; P < 0.05 vs aCSF). These data provide evidence of an endogenous forebrain GABAergic system which, when activated, can inhibit baroreceptor-mediated AVP release.

Original languageEnglish (US)
Pages (from-to)53-62
Number of pages10
JournalBrain Research
Volume499
Issue number1
DOIs
StatePublished - Oct 9 1989
Externally publishedYes

Fingerprint

Pressoreceptors
Arginine Vasopressin
Prosencephalon
Vasopressins
Chlorisondamine
Arterial Pressure
Enzyme Inhibitors
gamma-Aminobutyric Acid
GABA Uptake Inhibitors
Ganglionic Blockers
Controlled Hypotension
Aminobutyrates
Hypotension
Blood Vessels
Maintenance
nipecotic acid
Pressure
Injections

Keywords

  • Arginine-vasopressin
  • Baroreceptor
  • Cardiovascular regulation
  • Chlorisondamine
  • Converting enzyme inhibition
  • γ-Aminobutyric acid

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

Cite this

Evidence of an endogenous forebrain GABAergic system capable of inhibiting baroreceptor-mediated vasopressin release. / Segura, Ted; Hasser, Eileen M.; Shade, Robert E.; Haywood, Joseph R.

In: Brain Research, Vol. 499, No. 1, 09.10.1989, p. 53-62.

Research output: Contribution to journalArticle

Segura, Ted ; Hasser, Eileen M. ; Shade, Robert E. ; Haywood, Joseph R. / Evidence of an endogenous forebrain GABAergic system capable of inhibiting baroreceptor-mediated vasopressin release. In: Brain Research. 1989 ; Vol. 499, No. 1. pp. 53-62.
@article{f7695032413e429499b1bef1b0d8b438,
title = "Evidence of an endogenous forebrain GABAergic system capable of inhibiting baroreceptor-mediated vasopressin release",
abstract = "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) from 118±2 to 63±2 mm Hg, but pressure then rose to a compensated level of 78±1 mm 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 from 78±1 to 63±1 mm Hg. While AVP was contributing to MAP maintenance, GABA (15, 50 and 150 μg) caused dose-related reductions in MAP (5±1,7±1 and 11±2 mm Hg, respectively). Nipecotic acid (3-350 μg) also caused dose-related reductions in MAP (from 3±1 to 15±2 mm 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 by CEI + CHLOR and subsequent treatment with aCSF or nipecotic acid (175 μg). Hypotension induced by CEI + CHLOR caused a significant increase in pAVP. Forebrain-restricted nipecotic acid significantly suppressed pAVP (61 ± 8{\%} reduction; P < 0.05 vs aCSF). These data provide evidence of an endogenous forebrain GABAergic system which, when activated, can inhibit baroreceptor-mediated AVP release.",
keywords = "Arginine-vasopressin, Baroreceptor, Cardiovascular regulation, Chlorisondamine, Converting enzyme inhibition, γ-Aminobutyric acid",
author = "Ted Segura and Hasser, {Eileen M.} and Shade, {Robert E.} and Haywood, {Joseph R.}",
year = "1989",
month = "10",
day = "9",
doi = "10.1016/0006-8993(89)91134-7",
language = "English (US)",
volume = "499",
pages = "53--62",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - Evidence of an endogenous forebrain GABAergic system capable of inhibiting baroreceptor-mediated vasopressin release

AU - Segura, Ted

AU - Hasser, Eileen M.

AU - Shade, Robert E.

AU - Haywood, Joseph R.

PY - 1989/10/9

Y1 - 1989/10/9

N2 - 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) from 118±2 to 63±2 mm Hg, but pressure then rose to a compensated level of 78±1 mm 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 from 78±1 to 63±1 mm Hg. While AVP was contributing to MAP maintenance, GABA (15, 50 and 150 μg) caused dose-related reductions in MAP (5±1,7±1 and 11±2 mm Hg, respectively). Nipecotic acid (3-350 μg) also caused dose-related reductions in MAP (from 3±1 to 15±2 mm 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 by CEI + CHLOR and subsequent treatment with aCSF or nipecotic acid (175 μg). Hypotension induced by CEI + CHLOR caused a significant increase in pAVP. Forebrain-restricted nipecotic acid significantly suppressed pAVP (61 ± 8% reduction; P < 0.05 vs aCSF). These data provide evidence of an endogenous forebrain GABAergic system which, when activated, can inhibit baroreceptor-mediated AVP release.

AB - 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) from 118±2 to 63±2 mm Hg, but pressure then rose to a compensated level of 78±1 mm 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 from 78±1 to 63±1 mm Hg. While AVP was contributing to MAP maintenance, GABA (15, 50 and 150 μg) caused dose-related reductions in MAP (5±1,7±1 and 11±2 mm Hg, respectively). Nipecotic acid (3-350 μg) also caused dose-related reductions in MAP (from 3±1 to 15±2 mm 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 by CEI + CHLOR and subsequent treatment with aCSF or nipecotic acid (175 μg). Hypotension induced by CEI + CHLOR caused a significant increase in pAVP. Forebrain-restricted nipecotic acid significantly suppressed pAVP (61 ± 8% reduction; P < 0.05 vs aCSF). These data provide evidence of an endogenous forebrain GABAergic system which, when activated, can inhibit baroreceptor-mediated AVP release.

KW - Arginine-vasopressin

KW - Baroreceptor

KW - Cardiovascular regulation

KW - Chlorisondamine

KW - Converting enzyme inhibition

KW - γ-Aminobutyric acid

UR - http://www.scopus.com/inward/record.url?scp=0024424941&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024424941&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(89)91134-7

DO - 10.1016/0006-8993(89)91134-7

M3 - Article

C2 - 2804669

AN - SCOPUS:0024424941

VL - 499

SP - 53

EP - 62

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1

ER -