Abstract |
Previous studies have shown that CCK-8 has distinct antiopioid effect in the central sites related with pain control and blood pressure control. The aim of this study was to explore the receptor mechanism by which CCK-8 antagonized the depressor effect of u- and k- opioid agonists, and to observe whether CCK-8 could antagonize the depressor effect induced by muscimol, a nonopioid substance. The results showed that (i) The antagonistic effect of CCK-8 on opioid- induced hypotension could be blocked by intrathecal (i. t.) administration of CCK-B antagonist L-365, 260 at nanogram doses, or by CCK-A antagonist devazepide at doses 20-40 times higher than L-365, 260, indicating that it was the CCK-B receptor which mediates the antiopioid effect. (ii) The depressor effect induced by intrathecal muscimol, a GABA agonist, was blocked neither by naloxone nor by CCK-8, supporting the notion that CCK-8 is an endogenous opioid antagonist rather than a universal anti- hypotension agent.
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Authors | L Mei, J S Han |
Journal | Science in China. Series B, Chemistry, life sciences & earth sciences
(Sci China B)
Vol. 36
Issue 7
Pg. 817-23
(Jul 1993)
ISSN: 1001-652X [Print] China |
PMID | 8216742
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Benzodiazepinones
- Phenylurea Compounds
- Receptors, Cholecystokinin
- Muscimol
- L 365260
- Proglumide
- Devazepide
- Sincalide
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Topics |
- Animals
- Benzodiazepinones
(pharmacology)
- Blood Pressure
(drug effects)
- Devazepide
- Female
- Hypotension
(chemically induced, drug therapy)
- Muscimol
- Phenylurea Compounds
- Proglumide
(pharmacology)
- Rats
- Rats, Wistar
- Receptors, Cholecystokinin
(antagonists & inhibitors, physiology)
- Sincalide
(pharmacology, therapeutic use)
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