Receptor mechanism of infarct-limiting effect of adaptation to normobaric hypoxia

The aim of the study was to investigate the involvement of bradykinin, cannabinoid and vanilloid (TRPV1 channel) receptors in the implementation of the infarct-limiting effect of chronic normobaric hypoxia (CNH).Materials and methods. The study was performed on male Wistar rats (n = 117) weighing 25...

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Main Authors: N. V. Naryzhnaya, A. V. Mukhomedzyanov, S. Yu. Tsibulnikov, L. N. Maslov
Format: Article
Language:English
Published: Siberian State Medical University (Tomsk) 2021-01-01
Series:Бюллетень сибирской медицины
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Online Access:https://bulletin.ssmu.ru/jour/article/view/4161
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author N. V. Naryzhnaya
A. V. Mukhomedzyanov
S. Yu. Tsibulnikov
L. N. Maslov
author_facet N. V. Naryzhnaya
A. V. Mukhomedzyanov
S. Yu. Tsibulnikov
L. N. Maslov
author_sort N. V. Naryzhnaya
collection DOAJ
description The aim of the study was to investigate the involvement of bradykinin, cannabinoid and vanilloid (TRPV1 channel) receptors in the implementation of the infarct-limiting effect of chronic normobaric hypoxia (CNH).Materials and methods. The study was performed on male Wistar rats (n = 117) weighing 250–300 g. Adaptation to CNH was modeled for 21 days at 12% pO2, 0.3% pCO2 and normal atmospheric pressure. A day after adaptation of rats to CNH coronary artery occlusion (45 min) and reperfusion (2 h) was performed. In the study the following compounds were used: selective cannabinoid CB1 receptor antagonist rimonabant (1 mg/kg), selective cannabinoid CB2 receptor antagonist AM630 (2.5 mg/kg), selective bradykinin B2 receptor antagonist HOE140 (50 μg/kg), and vanilloid receptor (TRPV1 channel) antagonist capsazepine (3 mg/kg). All antagonists were administered 15 min before coronary artery occlusion.Results. Adaptation to normobaric hypoxia promoted the formation of the pronounced infarct-limiting effect.The blockade of B2 receptor eliminated the infarct-limiting effect of CNH. Blockade of cannabinoid or vanilloidreceptors did not affect the infarct-limiting effect of CNH.Conclusion. The infarct-limiting effect of CNH depends on the activation of B2 receptor, and the adaptive increase in cardiac tolerance to ischemia/reperfusion does not depend on cannabinoid or vanilloid receptors.
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spelling doaj-art-e4502de08cdf444783d4cf471d534cca2025-08-20T03:02:04ZengSiberian State Medical University (Tomsk)Бюллетень сибирской медицины1682-03631819-36842021-01-0119413814210.20538/1682-0363-2020-4-138-1422732Receptor mechanism of infarct-limiting effect of adaptation to normobaric hypoxiaN. V. Naryzhnaya0A. V. Mukhomedzyanov1S. Yu. Tsibulnikov2L. N. Maslov3Cardiology Research Institute, Tomsk National Research Medical Center (TNRMC), Russian Academy of ScienceCardiology Research Institute, Tomsk National Research Medical Center (TNRMC), Russian Academy of ScienceCardiology Research Institute, Tomsk National Research Medical Center (TNRMC), Russian Academy of ScienceCardiology Research Institute, Tomsk National Research Medical Center (TNRMC), Russian Academy of ScienceThe aim of the study was to investigate the involvement of bradykinin, cannabinoid and vanilloid (TRPV1 channel) receptors in the implementation of the infarct-limiting effect of chronic normobaric hypoxia (CNH).Materials and methods. The study was performed on male Wistar rats (n = 117) weighing 250–300 g. Adaptation to CNH was modeled for 21 days at 12% pO2, 0.3% pCO2 and normal atmospheric pressure. A day after adaptation of rats to CNH coronary artery occlusion (45 min) and reperfusion (2 h) was performed. In the study the following compounds were used: selective cannabinoid CB1 receptor antagonist rimonabant (1 mg/kg), selective cannabinoid CB2 receptor antagonist AM630 (2.5 mg/kg), selective bradykinin B2 receptor antagonist HOE140 (50 μg/kg), and vanilloid receptor (TRPV1 channel) antagonist capsazepine (3 mg/kg). All antagonists were administered 15 min before coronary artery occlusion.Results. Adaptation to normobaric hypoxia promoted the formation of the pronounced infarct-limiting effect.The blockade of B2 receptor eliminated the infarct-limiting effect of CNH. Blockade of cannabinoid or vanilloidreceptors did not affect the infarct-limiting effect of CNH.Conclusion. The infarct-limiting effect of CNH depends on the activation of B2 receptor, and the adaptive increase in cardiac tolerance to ischemia/reperfusion does not depend on cannabinoid or vanilloid receptors.https://bulletin.ssmu.ru/jour/article/view/4161myocardiumischemiareperfusionreceptorschronic hypoxia
spellingShingle N. V. Naryzhnaya
A. V. Mukhomedzyanov
S. Yu. Tsibulnikov
L. N. Maslov
Receptor mechanism of infarct-limiting effect of adaptation to normobaric hypoxia
Бюллетень сибирской медицины
myocardium
ischemia
reperfusion
receptors
chronic hypoxia
title Receptor mechanism of infarct-limiting effect of adaptation to normobaric hypoxia
title_full Receptor mechanism of infarct-limiting effect of adaptation to normobaric hypoxia
title_fullStr Receptor mechanism of infarct-limiting effect of adaptation to normobaric hypoxia
title_full_unstemmed Receptor mechanism of infarct-limiting effect of adaptation to normobaric hypoxia
title_short Receptor mechanism of infarct-limiting effect of adaptation to normobaric hypoxia
title_sort receptor mechanism of infarct limiting effect of adaptation to normobaric hypoxia
topic myocardium
ischemia
reperfusion
receptors
chronic hypoxia
url https://bulletin.ssmu.ru/jour/article/view/4161
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AT syutsibulnikov receptormechanismofinfarctlimitingeffectofadaptationtonormobarichypoxia
AT lnmaslov receptormechanismofinfarctlimitingeffectofadaptationtonormobarichypoxia