Participation of Opioid Receptors in the Cytoprotective Effect ofChronic Normobaric Hypoxia; Physiological Research; Vol. 68, iss. 2
| Parent link: | Physiological Research Vol. 68, iss. 2.— 2019.— [P. 245-253] |
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| Collectivité auteur: | |
| Autres auteurs: | , , , , , , |
| Résumé: | Title screen We studied the role of the δ, µ, and к opioid receptor (OR) subtypes in the cardioprotective effect of chronic continuous normobaric hypoxia (CNH) in the model of acuteanoxia/ reoxygenation of isolated cardiomyocytes. Adaptation of rats to CNH was performed by their exposure to atmosphere containing 12 % of O2 for 21 days. Anoxia/reoxygenation of cardiomyocytes isolated from normoxic control rats caused the death of 51 % of cells and lactate dehydrogenase (LDH) release. Adaptation of rats to CNH resulted in the anoxia/reoxygenation-induced cardiomyocyte death of only 38 %, and reduced the LDH release. Pre-incubation of the cells with either the non-selective OR blocker naloxone (300 nM/l), the δ OR antagonist TIPP(ψ) (30 nM/l), the selective δ2 OR antagonist naltriben (1 nM/l) or the μ OR antagonist CTAP (100 nM/l) for 25 minutes before anoxia abolished the reduction of cell death and LDH release afforded by CNH. The antagonist of δ1 OR BNTX (1 nM/l) or the κ OR antagonist nor-binaltorphimine (3 nM/l) did not influence the cytoprotective effects of CNH. Taken together, the cytoprotective effect of CNH is associated with the activation of the δ2 and μ OR localized on cardiomyocytes |
| Langue: | anglais |
| Publié: |
2019
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| Sujets: | |
| Accès en ligne: | https://doi.org/10.33549/physiolres.933938 |
| Format: | Électronique Chapitre de livre |
| KOHA link: | https://koha.lib.tpu.ru/cgi-bin/koha/opac-detail.pl?biblionumber=663260 |
| Résumé: | Title screen We studied the role of the δ, µ, and к opioid receptor (OR) subtypes in the cardioprotective effect of chronic continuous normobaric hypoxia (CNH) in the model of acuteanoxia/ reoxygenation of isolated cardiomyocytes. Adaptation of rats to CNH was performed by their exposure to atmosphere containing 12 % of O2 for 21 days. Anoxia/reoxygenation of cardiomyocytes isolated from normoxic control rats caused the death of 51 % of cells and lactate dehydrogenase (LDH) release. Adaptation of rats to CNH resulted in the anoxia/reoxygenation-induced cardiomyocyte death of only 38 %, and reduced the LDH release. Pre-incubation of the cells with either the non-selective OR blocker naloxone (300 nM/l), the δ OR antagonist TIPP(ψ) (30 nM/l), the selective δ2 OR antagonist naltriben (1 nM/l) or the μ OR antagonist CTAP (100 nM/l) for 25 minutes before anoxia abolished the reduction of cell death and LDH release afforded by CNH. The antagonist of δ1 OR BNTX (1 nM/l) or the κ OR antagonist nor-binaltorphimine (3 nM/l) did not influence the cytoprotective effects of CNH. Taken together, the cytoprotective effect of CNH is associated with the activation of the δ2 and μ OR localized on cardiomyocytes |
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| DOI: | 10.33549/physiolres.933938 |