Influence of glucocorticoids on cholinergic stimulation-induced catecholamine secretion from the rat adrenal medulla.
- Author:
Dong Yoon LIM
1
;
Jae Joon LEE
;
Oh Seong GWEON
Author Information
1. Department of Pharmacology, College of Medicine, Chosun University, Kwangju 501-759, Korea.
- Publication Type:Original Article
- Keywords:
Glucocorticoids;
Catecholamine Secretion;
Rat Adrenomedullary Chromaffin Cells
- MeSH:
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride;
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester;
Acetylcholine;
Adrenal Glands;
Adrenal Medulla*;
Animals;
Betamethasone;
Calcium;
Calcium Channels;
Catecholamines;
Chromaffin Cells;
Dexamethasone;
Dimethylphenylpiperazinium Iodide;
Glucocorticoids*;
Hydrocortisone;
Perfusion;
Rats*;
Receptors, Muscarinic;
Receptors, Nicotinic;
Veins
- From:The Korean Journal of Physiology and Pharmacology
1998;2(2):173-184
- CountryRepublic of Korea
- Language:English
-
Abstract:
The present study was undertaken to examine the influence of glucocorticoids on the secretory responses of catecholamines (CA) evoked by acetylcholine (ACh), DMPP, McN-A-343, excess K+ and Bay-K-8644 from the isolated perfused rat adrenal gland and to clarify the mechanism of its action. The perfusion of the synthetic glucocorticoid dexamethasone (10-100 micrometer) into an adrenal vein for 20 min produced a dose-dependent inhibition in CA secretion evoked by ACh (5.32 mM), excess K+ (a membrane-depolarizor 56 mM), DMPP (a selective nicotinic receptor agonist, 100 micrometer for 2 min), McN-A-343 (a muscarinic receptor agonist, 100 micrometer for 4 min), Bay-K-8644 (a calcium channel activator, 10 micrometer for 4 min) and cyclopiazonic acid (a releaser of intracellular Ca2+ 10 micrometer for 4 min). Similarly, the preperfusion of hydrocortisone (30 micrometer) for 20 min also attenuated significantly the secretory responses of CA evoked by nicotinic and muscarinic receptor stimulation as well as membrane-depolarization, Ca2+ channel activation and the release of intracellular Ca2+. Furthermore, even in the presence of betamethasone (30micrometer), CA secretion evoked by ACh, excess K+, DMPP and McN-A-343 was also markedly inhibited. Taken together, the present results suggest that glucocorticoids cause the marked inhibition of CA secretion evoked by both cholinergic nicotinic and muscarinic receptor stimulation from the isolated perfused rat adrenal gland, indicating strongly that this inhibitory effect may be mediated by inhibiting influx of extracellular calcium as well as the release of intracellular calcium in the rat adrenomedullary chromaffin cells.
