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
Open AccessConcept Paper

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
Pharmaceuticals 2015, 8(4), 664-674; https://doi.org/10.3390/ph8040664
Received: 16 August 2015 / Revised: 15 September 2015 / Accepted: 17 September 2015 / Published: 25 September 2015
(This article belongs to the Special Issue Choices of the Journal)
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
Show Figures

Figure 1

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

Article Access Map by Country/Region

1
Only visits after 24 November 2015 are recorded.
Back to TopTop