FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2040552632> ?p ?o ?g. }

• W2040552632 endingPage "510.e1" @default.
• W2040552632 startingPage "501" @default.
• W2040552632 abstract "ObjectivesEndothelial dysfunction occurs in hypoxia-related states such as ischemic heart disease or heart surgery. Intermediate- and small-conductance calcium-activated potassium channels (IKCa and SKCa) are closely related to endothelium-dependent hyperpolarizing factor–mediated endothelial function. However, the status of these KCa under hypoxia is unknown. We investigated whether endothelial dysfunction under hypoxic state is related to the alterations of IKCa and SKCa and whether use of IKCa/SKCa activator may protect endothelium from hypoxia–reoxygenation injury.MethodsIsometric tension measurement, patch-clamp technique, intracellular membrane potential recording, and molecular methods were used to study porcine coronary arteries and endothelial cells.ResultsHypoxia–reoxygenation (60–30 minutes) decreased endothelium-dependent hyperpolarizing factor–mediated relaxation at normothermia in Krebs solution (43.3% ± 6.3% vs 82.3% ± 2.9%) and in St Thomas' Hospital cardioplegic solution (28.9% ± 1.8% vs 78.1% ± 3.0%) (P < .001) as well as at hypothermia in St Thomas' Hospital solution (43.1% ± 2.6%, P < .001). Hypoxia–reoxygenation markedly reduced endothelial IKCa (2.8 ± 0.6 vs 6.9 ± 0.6 pA/pF) and SKCa currents (1.5 ± 0.3 vs 4.3 ± 0.4 pA/pF) (P < .05) and downregulated endothelial IKCa expression. IKCa/SKCa activator 1-ethyl-2-benzimidazolinone enhanced K+ current in endothelial cells that was blunted by hypoxia. Further, 1-ethyl-2-benzimidazolinone restored (P < .001) endothelium-dependent hyperpolarizing factor–mediated relaxation with hyperpolarization recovered from 6.0 ± 0.3 to 7.8 ± 0.4 mV (P < .05).ConclusionsIn porcine coronary arteries, hypoxia markedly reduced endothelial K+ currents related to IKCa and SKCa with downregulation of protein expression and endothelium-derived hyperpolarizing factor function. IKCa/SKCa activator may preserve endothelium-dependent hyperpolarizing factor–mediated relaxation with enhancement of K+ current in endothelial cells and cellular membrane potential hyperpolarization in smooth muscle cells and may become a new strategy to protect coronary endothelium in cardiac surgery or transplantation. Endothelial dysfunction occurs in hypoxia-related states such as ischemic heart disease or heart surgery. Intermediate- and small-conductance calcium-activated potassium channels (IKCa and SKCa) are closely related to endothelium-dependent hyperpolarizing factor–mediated endothelial function. However, the status of these KCa under hypoxia is unknown. We investigated whether endothelial dysfunction under hypoxic state is related to the alterations of IKCa and SKCa and whether use of IKCa/SKCa activator may protect endothelium from hypoxia–reoxygenation injury. Isometric tension measurement, patch-clamp technique, intracellular membrane potential recording, and molecular methods were used to study porcine coronary arteries and endothelial cells. Hypoxia–reoxygenation (60–30 minutes) decreased endothelium-dependent hyperpolarizing factor–mediated relaxation at normothermia in Krebs solution (43.3% ± 6.3% vs 82.3% ± 2.9%) and in St Thomas' Hospital cardioplegic solution (28.9% ± 1.8% vs 78.1% ± 3.0%) (P < .001) as well as at hypothermia in St Thomas' Hospital solution (43.1% ± 2.6%, P < .001). Hypoxia–reoxygenation markedly reduced endothelial IKCa (2.8 ± 0.6 vs 6.9 ± 0.6 pA/pF) and SKCa currents (1.5 ± 0.3 vs 4.3 ± 0.4 pA/pF) (P < .05) and downregulated endothelial IKCa expression. IKCa/SKCa activator 1-ethyl-2-benzimidazolinone enhanced K+ current in endothelial cells that was blunted by hypoxia. Further, 1-ethyl-2-benzimidazolinone restored (P < .001) endothelium-dependent hyperpolarizing factor–mediated relaxation with hyperpolarization recovered from 6.0 ± 0.3 to 7.8 ± 0.4 mV (P < .05). In porcine coronary arteries, hypoxia markedly reduced endothelial K+ currents related to IKCa and SKCa with downregulation of protein expression and endothelium-derived hyperpolarizing factor function. IKCa/SKCa activator may preserve endothelium-dependent hyperpolarizing factor–mediated relaxation with enhancement of K+ current in endothelial cells and cellular membrane potential hyperpolarization in smooth muscle cells and may become a new strategy to protect coronary endothelium in cardiac surgery or transplantation." @default.
• W2040552632 created "2016-06-24" @default.
• W2040552632 creator A5004387257 @default.
• W2040552632 creator A5011137129 @default.
• W2040552632 creator A5017713517 @default.
• W2040552632 creator A5039333280 @default.
• W2040552632 creator A5064231427 @default.
• W2040552632 date "2011-02-01" @default.
• W2040552632 modified "2023-10-04" @default.
• W2040552632 title "Use of intermediate/small conductance calcium-activated potassium-channel activator for endothelial protection" @default.
• W2040552632 cites W1534486598 @default.
• W2040552632 cites W1546802604 @default.
• W2040552632 cites W1963624422 @default.
• W2040552632 cites W1968135647 @default.
• W2040552632 cites W1979908346 @default.
• W2040552632 cites W1986407102 @default.
• W2040552632 cites W1987891633 @default.
• W2040552632 cites W1998309193 @default.
• W2040552632 cites W2005285935 @default.
• W2040552632 cites W2007644118 @default.
• W2040552632 cites W2007737411 @default.
• W2040552632 cites W2012012271 @default.
• W2040552632 cites W2021403302 @default.
• W2040552632 cites W2039463488 @default.
• W2040552632 cites W2062050978 @default.
• W2040552632 cites W2065906335 @default.
• W2040552632 cites W2067474104 @default.
• W2040552632 cites W2074481216 @default.
• W2040552632 cites W2082535977 @default.
• W2040552632 cites W2092145002 @default.
• W2040552632 cites W2104569461 @default.
• W2040552632 cites W2105050513 @default.
• W2040552632 cites W2126029591 @default.
• W2040552632 cites W2135579766 @default.
• W2040552632 cites W2137962262 @default.
• W2040552632 cites W2147061390 @default.
• W2040552632 cites W2152982406 @default.
• W2040552632 cites W2157361092 @default.
• W2040552632 cites W2166425022 @default.
• W2040552632 cites W2412551193 @default.
• W2040552632 cites W2415206848 @default.
• W2040552632 cites W2415762300 @default.
• W2040552632 doi "https://doi.org/10.1016/j.jtcvs.2010.04.005" @default.
• W2040552632 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20546794" @default.
• W2040552632 hasPublicationYear "2011" @default.
• W2040552632 type Work @default.
• W2040552632 sameAs 2040552632 @default.
• W2040552632 citedByCount "37" @default.
• W2040552632 countsByYear W20405526322012 @default.
• W2040552632 countsByYear W20405526322013 @default.
• W2040552632 countsByYear W20405526322014 @default.
• W2040552632 countsByYear W20405526322015 @default.
• W2040552632 countsByYear W20405526322016 @default.
• W2040552632 countsByYear W20405526322017 @default.
• W2040552632 countsByYear W20405526322018 @default.
• W2040552632 countsByYear W20405526322019 @default.
• W2040552632 countsByYear W20405526322020 @default.
• W2040552632 countsByYear W20405526322021 @default.
• W2040552632 countsByYear W20405526322022 @default.
• W2040552632 crossrefType "journal-article" @default.
• W2040552632 hasAuthorship W2040552632A5004387257 @default.
• W2040552632 hasAuthorship W2040552632A5011137129 @default.
• W2040552632 hasAuthorship W2040552632A5017713517 @default.
• W2040552632 hasAuthorship W2040552632A5039333280 @default.
• W2040552632 hasAuthorship W2040552632A5064231427 @default.
• W2040552632 hasBestOaLocation W20405526321 @default.
• W2040552632 hasConcept C126322002 @default.
• W2040552632 hasConcept C131453863 @default.
• W2040552632 hasConcept C134018914 @default.
• W2040552632 hasConcept C149614440 @default.
• W2040552632 hasConcept C178790620 @default.
• W2040552632 hasConcept C185592680 @default.
• W2040552632 hasConcept C2776919887 @default.
• W2040552632 hasConcept C2776992346 @default.
• W2040552632 hasConcept C2779411790 @default.
• W2040552632 hasConcept C2780972559 @default.
• W2040552632 hasConcept C42219234 @default.
• W2040552632 hasConcept C540031477 @default.
• W2040552632 hasConcept C66974803 @default.
• W2040552632 hasConcept C71924100 @default.
• W2040552632 hasConcept C7836513 @default.
• W2040552632 hasConcept C83743174 @default.
• W2040552632 hasConcept C98274493 @default.
• W2040552632 hasConceptScore W2040552632C126322002 @default.
• W2040552632 hasConceptScore W2040552632C131453863 @default.
• W2040552632 hasConceptScore W2040552632C134018914 @default.
• W2040552632 hasConceptScore W2040552632C149614440 @default.
• W2040552632 hasConceptScore W2040552632C178790620 @default.
• W2040552632 hasConceptScore W2040552632C185592680 @default.
• W2040552632 hasConceptScore W2040552632C2776919887 @default.
• W2040552632 hasConceptScore W2040552632C2776992346 @default.
• W2040552632 hasConceptScore W2040552632C2779411790 @default.
• W2040552632 hasConceptScore W2040552632C2780972559 @default.
• W2040552632 hasConceptScore W2040552632C42219234 @default.
• W2040552632 hasConceptScore W2040552632C540031477 @default.
• W2040552632 hasConceptScore W2040552632C66974803 @default.
• W2040552632 hasConceptScore W2040552632C71924100 @default.
• W2040552632 hasConceptScore W2040552632C7836513 @default.

• next