Participation of Opioid Receptors in the Cytoprotective Effect ofChronic Normobaric Hypoxia

Bibliographic Details
Parent link:Physiological Research
Vol. 68, iss. 2.— 2019.— [P. 245-253]
Corporate Author: Национальный исследовательский Томский политехнический университет Физико-технический институт Лаборатория № 31 ядерного реактора
Other Authors: Naryzhnaya N. V. Nataliya Vladimirovna, Khaliulin I. G. Igor Grigorjevich, Lishmanov Yu. B. Yury Borisovich, Suleiman M. S. Saadeh, Tsybulnikov S. Yu. Sergey Yurjevich, Kolar F. Frantisek, Maslov L. N. Leonid Nikolaevich
Summary: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
Language:English
Published: 2019
Subjects:
Online Access:https://doi.org/10.33549/physiolres.933938
Format: Electronic Book Chapter
KOHA link:https://koha.lib.tpu.ru/cgi-bin/koha/opac-detail.pl?biblionumber=663260