Next Article in Journal
Mitochondrial Dysfunction and Disturbed Coherence: Gate to Cancer
Next Article in Special Issue
29ièmes Journées Franco-Belges de Pharmacochimie: Meeting Report
Previous Article in Journal
Pharmacogenomics Implications of Using Herbal Medicinal Plants on African Populations in Health Transition
Previous Article in Special Issue
Antimicrobial Peptides in 2014
Article Menu

Export Article

Open AccessConcept Paper
Pharmaceuticals 2015, 8(4), 664-674; doi:10.3390/ph8040664

Opioid Facilitation of β-Adrenergic Blockade: A New Pharmacological Condition?

1
Inserm, Laboratory of Molecular Biology and Biochemistry, Hormonology Metabolism Nutrition and Oncology, Center of Biology and Pathology, CHRU Lille, and RADEME EA 7364, Faculty of Medicine, University of Lille 2, Lille 59037, France
2
Centre de Référence Maladies Héréditaires du Métabolisme de l'Enfant et de l'Adulte, Jeanne de Flandre Hospital, CHRU Lille, and RADEME EA 7364, Faculty of Medicine, University Lille 2, Lille 59037, France
3
Pediatric Critical Care Unit, Hôpital Jeanne de Flandre, CHRU Lille, Lille 59037, France
*
Author to whom correspondence should be addressed.
Academic Editor: Jean Jacques Vanden Eynde
Received: 16 August 2015 / Revised: 15 September 2015 / Accepted: 17 September 2015 / Published: 25 September 2015
(This article belongs to the Collection Choices of the Journal)
View Full-Text   |   Download PDF [610 KB, uploaded 25 September 2015]   |  

Abstract

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. View Full-Text
Keywords: lactate; glycolysis disruption; Na+/K+ ATPase; β-adrenergic receptor; G protein; cAMP; protein kinase A; shock; δ-opioid receptor lactate; glycolysis disruption; Na+/K+ ATPase; β-adrenergic receptor; G protein; cAMP; protein kinase A; shock; δ-opioid receptor
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Vamecq, J.; Mention-Mulliez, K.; Leclerc, F.; Dobbelaere, D. Opioid Facilitation of β-Adrenergic Blockade: A New Pharmacological Condition? Pharmaceuticals 2015, 8, 664-674.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Pharmaceuticals EISSN 1424-8247 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top