• Eszter Szlavicz, Pannilage Shiromi Perera, Csaba Tomboly, Zsuzsanna Helyes, Ferenc Zador, Sandor Benyhe, Anna Borsodi, and Engin Bojnik.
• From the *Laboratory of Opioid Research, Institute of Biochemistry, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary; †Faculty of Medicine, University of Kelaniya, Ragama, Sri Lanka; and ‡Department of Pharmacology and Pharmacotherapy, Medical School Pecs, Pecs, Hungary.
• Anesth. Analg. 2015 Dec 1;121(6):1488-94.

BackgroundHemopressin, so-called because of its hypotensive effect, belongs to the derivatives of the hemoglobin α-chain. It was isolated from rat brain membrane homogenate by the use of catalytically inactive forms of endopeptidase 24.15 and neurolysin. Hemopressin has antihyperalgesic features that cannot be prevented by the opioid receptor antagonist, naloxone.MethodsIn the present study, we investigated whether hemopressin (PVNFKFLSH) and its C-terminally truncated fragment hemopressin 1-7 (PVNFKFL) have any influence on opioid-dependent signaling. Peptides have been analyzed using G-protein-stimulating functional and receptor bindings in this experimental setup.ResultsThese 2 compounds efficiently activated the G-proteins, and naloxone slightly blocked this stimulation. At the same time, they were able to displace radiolabeled [3H]DAMGO, a selective ligand for μ-opioid system, at micromolar concentrations. Displacement caused by the heptapeptide was more modest compared with hemopressin. Experiments performed on cell lines overexpressing μ-opioid receptors verified the opioid activity of both hemopressins. Moreover, the CB1 cannabinoid receptor antagonist, AM251, significantly decreased their G-protein stimulatory effect.ConclusionsHere, we further confirm that hemopressins can modulate CB1 receptors and can have a slight modulatory effect on the opioid system.

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