Korean J Physiol Pharmacol.
1998 Apr;2(2):173-184.
Influence of glucocorticoids on cholinergic stimulation-induced catecholamine secretion from the rat adrenal medulla
- Affiliations
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- 1Department of Pharmacology, College of Medicine, Chosun University, Kwangju 501-759, Korea.
Abstract
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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.