Bibliographic Details
Title: |
Opioid Facilitation of β-Adrenergic Blockade: A New Pharmacological Condition? |
Authors: |
Joseph Vamecq, Karine Mention-Mulliez, Francis Leclerc, Dries Dobbelaere |
Source: |
Pharmaceuticals, Vol 8, Iss 4, Pp 664-674 (2015) |
Publisher Information: |
MDPI AG, 2015. |
Publication Year: |
2015 |
Collection: |
LCC:Medicine LCC:Pharmacy and materia medica |
Subject Terms: |
lactate, glycolysis disruption, Na+/K+ ATPase, β-adrenergic receptor, G protein, cAMP, protein kinase A, shock, δ-opioid receptor, Medicine, Pharmacy and materia medica, RS1-441 |
More Details: |
Recently, propranolol was suggested to prevent hyperlactatemia in a child with hypovolemic shock through β-adrenergic blockade. Though it is a known inhibitor of glycolysis, propranolol, outside this observation, has never been reported to fully protect against lactate overproduction. On the other hand, literature evidence exists for a cross-talk between β-adrenergic receptors (protein targets of propranolol) and δ-opioid receptor. In this literature context, it is hypothesized here that anti-diarrheic racecadotril (a pro-drug of thiorphan, an inhibitor of enkephalinases), which, in the cited observation, was co-administered with propranolol, might have facilitated the β-blocker-driven inhibition of glycolysis and resulting lactate production. The opioid-facilitated β-adrenergic blockade would be essentially additivity or even synergism putatively existing between antagonism of β-adrenergic receptors and agonism of δ-opioid receptor in lowering cellular cAMP and dependent functions. |
Document Type: |
article |
File Description: |
electronic resource |
Language: |
English |
ISSN: |
1424-8247 |
Relation: |
http://www.mdpi.com/1424-8247/8/4/664; https://doaj.org/toc/1424-8247 |
DOI: |
10.3390/ph8040664 |
Access URL: |
https://doaj.org/article/e95a6400a45f4739913037a05d99ae7d |
Accession Number: |
edsdoj.95a6400a45f4739913037a05d99ae7d |
Database: |
Directory of Open Access Journals |