Influence of GABAergic Receptors on Catecholamine Secretion in the Isolated Rat Adrenal Glands.
10.4070/kcj.1995.25.6.1197
- Author:
Soon Pyo HONG
;
Dong Yoon LIM
;
Jin Hee OH
;
Cheol hee CHOI
;
Ho Jin YOO
;
Jae Joon LEE
;
Jae Bong HEO
;
Young JANG
;
Jin Ho KIM
;
Jeong Won KANG
- Publication Type:Original Article
- Keywords:
GABAregic A-receptors;
Catecholamine Secretion;
Adrenal Gland
- MeSH:
Adrenal Glands*;
Animals;
Atropine;
Bicuculline;
Blood Vessels;
Calcium;
Catheters;
Central Nervous System;
Ether;
gamma-Aminobutyric Acid;
Humans;
Male;
Mecamylamine;
Neurotransmitter Agents;
Ouabain;
Perfusion;
Picrotoxin;
Potassium;
Rats*;
Rats, Sprague-Dawley;
Renal Veins;
Tachyphylaxis;
Veins
- From:Korean Circulation Journal
1995;25(6):1197-1207
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The influence of gamma-aminobutyric acid(GABA), which is well-known as a major inhibitory neurotransmitter in central nervous system, on secretion of catecholamines(CA) was investigated in the isolated perfused rat adrenal gland. METHODS: Mature male Sprague-Dawley rats were anesthetized with ether. Ther adrenal gland was isolated by the methods f Wakade. A cannula used for perfusion of the adrenal gladn was inserted into the distal end of the renal vein. The adrenal gland, along with ligated blood vessels and the cannula, was carefully removed from the animal and placed on a platform of a leucite chamber. RESULTS: GABA given into an adrenal vein of the rat produced markedly secretion of CA from the adrenal gland. Tachyphylaxis to the relesing effect of CA evoked by GABA was observed. The secretory effect of CA evoked by GABA was attenuated singnificantly by pretreatment with mecamylamine or atropine. Ouabain inhibited greatly the secretory response of GABA. When omitting the external potassium ion, the basal release of CA was increased. During this period GABA no longer revealed the increase in CA release. CA secretion evoked by GABA was blocked significantly by perfusion of calcium-free Krebs solution containing 5mMEGTA for 30-min. Pretreatment with bicuculline or picrotoxin inhibited CA secretion evoked by GABA as well as ACh. ACh-evoked CA release was potentiated by GABA infusion(400ug/30min). CONCLUSION: The experimental findings suggest that GABA causes the secretory effect of CA in a fashion of external calcium and potassium iosn-dependence, and that this releasing effect of CA induced by GABA may be exterted by stimulation of GABAergic A-reccptors located on adrenomedullary chromaffine cell, which is likely associated with cholinergic receptor activation evoked CA secretion.
