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Influence of naloxone on catecholamine release evoked by nicotinic receptor stimulation in the isolated rat adrenal gland

Influence of naloxone on catecholamine release evoked by nicotinic receptor stimulation in the... The present study was designed to investigate the effect of naloxone, a well known opioid antagonist, on the secretion of catecholamines (CA) evoked by cholinergic stimulation and membrane-depolarization in the isolated perfused rat adrenal glands, and to establish its mechanism of action. Naloxone (10 −6 ∼10 −5 M), perfused into an adrenal vein for 60 min, produced dose- and time-dependent inhibition of CA secretory responses evoked by ACh (5.32×10 −3 M), high K + (5.6×10 −2 M), DMPP (10 −4 M) and McN-A-343 (10 −4 M). Naloxone itself also failed to affect the basal CA output. In adrenal glands loaded with naloxone (3×10 −6 M), the CA secretory responses evoked by Bay-K-8644, an activator of l -type Ca 2+ channels, and cyclopiazonic acid, an inhibitor of cytoplasmic Ca 2+ -ATPase, were also inhibited. In the presence of met-enkephalin (5×10 −6 M), a well known opioid agonist, the CA secretory responses evoked by ACh, high K + , DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly inhibited. Taken together, these results suggest that naloxone greatly inhibits the CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as that by membrane depolarization. It seems that these inhibitory effects of naloxone does not involve opioid receptors, but might be mediated by blocking both the calcium influx into the rat adrenal medullary chromaffin cells and the uptake of Ca 2+ into the cytoplasmic calcium store, which are at least partly relevant to the direct interaction with the nicotinic receptor itself. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Pharmacal Research Springer Journals

Influence of naloxone on catecholamine release evoked by nicotinic receptor stimulation in the isolated rat adrenal gland

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References (44)

Publisher
Springer Journals
Copyright
Copyright © 2005 by The Pharmaceutical Society of Korea
Subject
Pharmacy; Pharmacy; Pharmacology/Toxicology
ISSN
0253-6269
eISSN
1976-3786
DOI
10.1007/BF02969361
Publisher site
See Article on Publisher Site

Abstract

The present study was designed to investigate the effect of naloxone, a well known opioid antagonist, on the secretion of catecholamines (CA) evoked by cholinergic stimulation and membrane-depolarization in the isolated perfused rat adrenal glands, and to establish its mechanism of action. Naloxone (10 −6 ∼10 −5 M), perfused into an adrenal vein for 60 min, produced dose- and time-dependent inhibition of CA secretory responses evoked by ACh (5.32×10 −3 M), high K + (5.6×10 −2 M), DMPP (10 −4 M) and McN-A-343 (10 −4 M). Naloxone itself also failed to affect the basal CA output. In adrenal glands loaded with naloxone (3×10 −6 M), the CA secretory responses evoked by Bay-K-8644, an activator of l -type Ca 2+ channels, and cyclopiazonic acid, an inhibitor of cytoplasmic Ca 2+ -ATPase, were also inhibited. In the presence of met-enkephalin (5×10 −6 M), a well known opioid agonist, the CA secretory responses evoked by ACh, high K + , DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly inhibited. Taken together, these results suggest that naloxone greatly inhibits the CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as that by membrane depolarization. It seems that these inhibitory effects of naloxone does not involve opioid receptors, but might be mediated by blocking both the calcium influx into the rat adrenal medullary chromaffin cells and the uptake of Ca 2+ into the cytoplasmic calcium store, which are at least partly relevant to the direct interaction with the nicotinic receptor itself.

Journal

Archives of Pharmacal ResearchSpringer Journals

Published: Jun 1, 2005

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