Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat
Aims: The transient receptor potential canonical channel 1 (TRPC1) is a crucial component of the stretch-activated ion channels (SACs). The objective of this research was to demonstrate the contribution of TRPC1 in maintaining cardiac contractile function in the hypertrophic myocardium. Methods: Hyp...
Ausführliche Beschreibung
Autor*in: |
Mo-Si Chen [verfasserIn] Jun-Hua Xiao [verfasserIn] Yong Wang [verfasserIn] Bo-Ming Xu [verfasserIn] Lu Gao [verfasserIn] Jia-Ling Wang [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2013 |
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Schlagwörter: |
Transient receptor potential canonical channel 1 |
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Übergeordnetes Werk: |
In: Cellular Physiology and Biochemistry - Cell Physiol Biochem Press GmbH & Co KG, 2002, 32(2013), 4, Seite 951-959 |
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Übergeordnetes Werk: |
volume:32 ; year:2013 ; number:4 ; pages:951-959 |
Links: |
Link aufrufen |
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DOI / URN: |
10.1159/000354498 |
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Katalog-ID: |
DOAJ023683996 |
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520 | |a Aims: The transient receptor potential canonical channel 1 (TRPC1) is a crucial component of the stretch-activated ion channels (SACs). The objective of this research was to demonstrate the contribution of TRPC1 in maintaining cardiac contractile function in the hypertrophic myocardium. Methods: Hypertrophic rat hearts were induced by injecting isoproterenol intraperitoneally, and the expressions of TRPC1/3/6 and Na+/Ca2+ exchanger 1 (NCX1) proteins were analyzed by Western blot. The intracellular calcium images, the action potential of myocardium, the length-dependent contractile force of ventricle muscle and the cardiac output of isolated heart were investigated. Results: The expression of TRPC1 was increased in the hypertrophic myocardium. After being stretched, the ascendant amplitude of the increase in the intracellular calcium ion concentration ([Ca2+]i) in the hypertrophic myocardium was higher than that in the normal myocardium. The increase of the APD50 and the amplitude of the membrane potential depolarization were more significant in the hypertrophic myocardium after the activation of SACs. When the heart preparations were perfused with Tyrode's solution, there was no difference in the cardiac systolic function between the cardiac hypertrophy group and the control group. Gadolinium, a SACs blocker, reduced the length-dependent contractile force and suppressed the ascending limb of the Frank-Starling curves in the hypertrophic heart. Conclusions: The upregulation of TRPC1 contributes to the contractile function in the hypertrophic myocardium by increasing [Ca2+]i through the SACs. | ||
650 | 4 | |a Transient receptor potential canonical channel 1 | |
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650 | 4 | |a Hypertrophic myocardium | |
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10.1159/000354498 doi (DE-627)DOAJ023683996 (DE-599)DOAJ98ae924bab074131946028b713a9f814 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Mo-Si Chen verfasserin aut Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims: The transient receptor potential canonical channel 1 (TRPC1) is a crucial component of the stretch-activated ion channels (SACs). The objective of this research was to demonstrate the contribution of TRPC1 in maintaining cardiac contractile function in the hypertrophic myocardium. Methods: Hypertrophic rat hearts were induced by injecting isoproterenol intraperitoneally, and the expressions of TRPC1/3/6 and Na+/Ca2+ exchanger 1 (NCX1) proteins were analyzed by Western blot. The intracellular calcium images, the action potential of myocardium, the length-dependent contractile force of ventricle muscle and the cardiac output of isolated heart were investigated. Results: The expression of TRPC1 was increased in the hypertrophic myocardium. After being stretched, the ascendant amplitude of the increase in the intracellular calcium ion concentration ([Ca2+]i) in the hypertrophic myocardium was higher than that in the normal myocardium. The increase of the APD50 and the amplitude of the membrane potential depolarization were more significant in the hypertrophic myocardium after the activation of SACs. When the heart preparations were perfused with Tyrode's solution, there was no difference in the cardiac systolic function between the cardiac hypertrophy group and the control group. Gadolinium, a SACs blocker, reduced the length-dependent contractile force and suppressed the ascending limb of the Frank-Starling curves in the hypertrophic heart. Conclusions: The upregulation of TRPC1 contributes to the contractile function in the hypertrophic myocardium by increasing [Ca2+]i through the SACs. Transient receptor potential canonical channel 1 Stretch-activated ion channels Hypertrophic myocardium Contractile function Physiology Biochemistry Jun-Hua Xiao verfasserin aut Yong Wang verfasserin aut Bo-Ming Xu verfasserin aut Lu Gao verfasserin aut Jia-Ling Wang verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 32(2013), 4, Seite 951-959 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:32 year:2013 number:4 pages:951-959 https://doi.org/10.1159/000354498 kostenfrei https://doaj.org/article/98ae924bab074131946028b713a9f814 kostenfrei http://www.karger.com/Article/FullText/354498 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 32 2013 4 951-959 |
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10.1159/000354498 doi (DE-627)DOAJ023683996 (DE-599)DOAJ98ae924bab074131946028b713a9f814 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Mo-Si Chen verfasserin aut Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims: The transient receptor potential canonical channel 1 (TRPC1) is a crucial component of the stretch-activated ion channels (SACs). The objective of this research was to demonstrate the contribution of TRPC1 in maintaining cardiac contractile function in the hypertrophic myocardium. Methods: Hypertrophic rat hearts were induced by injecting isoproterenol intraperitoneally, and the expressions of TRPC1/3/6 and Na+/Ca2+ exchanger 1 (NCX1) proteins were analyzed by Western blot. The intracellular calcium images, the action potential of myocardium, the length-dependent contractile force of ventricle muscle and the cardiac output of isolated heart were investigated. Results: The expression of TRPC1 was increased in the hypertrophic myocardium. After being stretched, the ascendant amplitude of the increase in the intracellular calcium ion concentration ([Ca2+]i) in the hypertrophic myocardium was higher than that in the normal myocardium. The increase of the APD50 and the amplitude of the membrane potential depolarization were more significant in the hypertrophic myocardium after the activation of SACs. When the heart preparations were perfused with Tyrode's solution, there was no difference in the cardiac systolic function between the cardiac hypertrophy group and the control group. Gadolinium, a SACs blocker, reduced the length-dependent contractile force and suppressed the ascending limb of the Frank-Starling curves in the hypertrophic heart. Conclusions: The upregulation of TRPC1 contributes to the contractile function in the hypertrophic myocardium by increasing [Ca2+]i through the SACs. Transient receptor potential canonical channel 1 Stretch-activated ion channels Hypertrophic myocardium Contractile function Physiology Biochemistry Jun-Hua Xiao verfasserin aut Yong Wang verfasserin aut Bo-Ming Xu verfasserin aut Lu Gao verfasserin aut Jia-Ling Wang verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 32(2013), 4, Seite 951-959 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:32 year:2013 number:4 pages:951-959 https://doi.org/10.1159/000354498 kostenfrei https://doaj.org/article/98ae924bab074131946028b713a9f814 kostenfrei http://www.karger.com/Article/FullText/354498 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 32 2013 4 951-959 |
allfields_unstemmed |
10.1159/000354498 doi (DE-627)DOAJ023683996 (DE-599)DOAJ98ae924bab074131946028b713a9f814 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Mo-Si Chen verfasserin aut Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims: The transient receptor potential canonical channel 1 (TRPC1) is a crucial component of the stretch-activated ion channels (SACs). The objective of this research was to demonstrate the contribution of TRPC1 in maintaining cardiac contractile function in the hypertrophic myocardium. Methods: Hypertrophic rat hearts were induced by injecting isoproterenol intraperitoneally, and the expressions of TRPC1/3/6 and Na+/Ca2+ exchanger 1 (NCX1) proteins were analyzed by Western blot. The intracellular calcium images, the action potential of myocardium, the length-dependent contractile force of ventricle muscle and the cardiac output of isolated heart were investigated. Results: The expression of TRPC1 was increased in the hypertrophic myocardium. After being stretched, the ascendant amplitude of the increase in the intracellular calcium ion concentration ([Ca2+]i) in the hypertrophic myocardium was higher than that in the normal myocardium. The increase of the APD50 and the amplitude of the membrane potential depolarization were more significant in the hypertrophic myocardium after the activation of SACs. When the heart preparations were perfused with Tyrode's solution, there was no difference in the cardiac systolic function between the cardiac hypertrophy group and the control group. Gadolinium, a SACs blocker, reduced the length-dependent contractile force and suppressed the ascending limb of the Frank-Starling curves in the hypertrophic heart. Conclusions: The upregulation of TRPC1 contributes to the contractile function in the hypertrophic myocardium by increasing [Ca2+]i through the SACs. Transient receptor potential canonical channel 1 Stretch-activated ion channels Hypertrophic myocardium Contractile function Physiology Biochemistry Jun-Hua Xiao verfasserin aut Yong Wang verfasserin aut Bo-Ming Xu verfasserin aut Lu Gao verfasserin aut Jia-Ling Wang verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 32(2013), 4, Seite 951-959 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:32 year:2013 number:4 pages:951-959 https://doi.org/10.1159/000354498 kostenfrei https://doaj.org/article/98ae924bab074131946028b713a9f814 kostenfrei http://www.karger.com/Article/FullText/354498 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 32 2013 4 951-959 |
allfieldsGer |
10.1159/000354498 doi (DE-627)DOAJ023683996 (DE-599)DOAJ98ae924bab074131946028b713a9f814 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Mo-Si Chen verfasserin aut Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims: The transient receptor potential canonical channel 1 (TRPC1) is a crucial component of the stretch-activated ion channels (SACs). The objective of this research was to demonstrate the contribution of TRPC1 in maintaining cardiac contractile function in the hypertrophic myocardium. Methods: Hypertrophic rat hearts were induced by injecting isoproterenol intraperitoneally, and the expressions of TRPC1/3/6 and Na+/Ca2+ exchanger 1 (NCX1) proteins were analyzed by Western blot. The intracellular calcium images, the action potential of myocardium, the length-dependent contractile force of ventricle muscle and the cardiac output of isolated heart were investigated. Results: The expression of TRPC1 was increased in the hypertrophic myocardium. After being stretched, the ascendant amplitude of the increase in the intracellular calcium ion concentration ([Ca2+]i) in the hypertrophic myocardium was higher than that in the normal myocardium. The increase of the APD50 and the amplitude of the membrane potential depolarization were more significant in the hypertrophic myocardium after the activation of SACs. When the heart preparations were perfused with Tyrode's solution, there was no difference in the cardiac systolic function between the cardiac hypertrophy group and the control group. Gadolinium, a SACs blocker, reduced the length-dependent contractile force and suppressed the ascending limb of the Frank-Starling curves in the hypertrophic heart. Conclusions: The upregulation of TRPC1 contributes to the contractile function in the hypertrophic myocardium by increasing [Ca2+]i through the SACs. Transient receptor potential canonical channel 1 Stretch-activated ion channels Hypertrophic myocardium Contractile function Physiology Biochemistry Jun-Hua Xiao verfasserin aut Yong Wang verfasserin aut Bo-Ming Xu verfasserin aut Lu Gao verfasserin aut Jia-Ling Wang verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 32(2013), 4, Seite 951-959 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:32 year:2013 number:4 pages:951-959 https://doi.org/10.1159/000354498 kostenfrei https://doaj.org/article/98ae924bab074131946028b713a9f814 kostenfrei http://www.karger.com/Article/FullText/354498 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 32 2013 4 951-959 |
allfieldsSound |
10.1159/000354498 doi (DE-627)DOAJ023683996 (DE-599)DOAJ98ae924bab074131946028b713a9f814 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Mo-Si Chen verfasserin aut Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims: The transient receptor potential canonical channel 1 (TRPC1) is a crucial component of the stretch-activated ion channels (SACs). The objective of this research was to demonstrate the contribution of TRPC1 in maintaining cardiac contractile function in the hypertrophic myocardium. Methods: Hypertrophic rat hearts were induced by injecting isoproterenol intraperitoneally, and the expressions of TRPC1/3/6 and Na+/Ca2+ exchanger 1 (NCX1) proteins were analyzed by Western blot. The intracellular calcium images, the action potential of myocardium, the length-dependent contractile force of ventricle muscle and the cardiac output of isolated heart were investigated. Results: The expression of TRPC1 was increased in the hypertrophic myocardium. After being stretched, the ascendant amplitude of the increase in the intracellular calcium ion concentration ([Ca2+]i) in the hypertrophic myocardium was higher than that in the normal myocardium. The increase of the APD50 and the amplitude of the membrane potential depolarization were more significant in the hypertrophic myocardium after the activation of SACs. When the heart preparations were perfused with Tyrode's solution, there was no difference in the cardiac systolic function between the cardiac hypertrophy group and the control group. Gadolinium, a SACs blocker, reduced the length-dependent contractile force and suppressed the ascending limb of the Frank-Starling curves in the hypertrophic heart. Conclusions: The upregulation of TRPC1 contributes to the contractile function in the hypertrophic myocardium by increasing [Ca2+]i through the SACs. Transient receptor potential canonical channel 1 Stretch-activated ion channels Hypertrophic myocardium Contractile function Physiology Biochemistry Jun-Hua Xiao verfasserin aut Yong Wang verfasserin aut Bo-Ming Xu verfasserin aut Lu Gao verfasserin aut Jia-Ling Wang verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 32(2013), 4, Seite 951-959 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:32 year:2013 number:4 pages:951-959 https://doi.org/10.1159/000354498 kostenfrei https://doaj.org/article/98ae924bab074131946028b713a9f814 kostenfrei http://www.karger.com/Article/FullText/354498 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 32 2013 4 951-959 |
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Mo-Si Chen misc QP1-981 misc QD415-436 misc Transient receptor potential canonical channel 1 misc Stretch-activated ion channels misc Hypertrophic myocardium misc Contractile function misc Physiology misc Biochemistry Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat |
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QP1-981 QD415-436 Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat Transient receptor potential canonical channel 1 Stretch-activated ion channels Hypertrophic myocardium Contractile function |
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Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat |
abstract |
Aims: The transient receptor potential canonical channel 1 (TRPC1) is a crucial component of the stretch-activated ion channels (SACs). The objective of this research was to demonstrate the contribution of TRPC1 in maintaining cardiac contractile function in the hypertrophic myocardium. Methods: Hypertrophic rat hearts were induced by injecting isoproterenol intraperitoneally, and the expressions of TRPC1/3/6 and Na+/Ca2+ exchanger 1 (NCX1) proteins were analyzed by Western blot. The intracellular calcium images, the action potential of myocardium, the length-dependent contractile force of ventricle muscle and the cardiac output of isolated heart were investigated. Results: The expression of TRPC1 was increased in the hypertrophic myocardium. After being stretched, the ascendant amplitude of the increase in the intracellular calcium ion concentration ([Ca2+]i) in the hypertrophic myocardium was higher than that in the normal myocardium. The increase of the APD50 and the amplitude of the membrane potential depolarization were more significant in the hypertrophic myocardium after the activation of SACs. When the heart preparations were perfused with Tyrode's solution, there was no difference in the cardiac systolic function between the cardiac hypertrophy group and the control group. Gadolinium, a SACs blocker, reduced the length-dependent contractile force and suppressed the ascending limb of the Frank-Starling curves in the hypertrophic heart. Conclusions: The upregulation of TRPC1 contributes to the contractile function in the hypertrophic myocardium by increasing [Ca2+]i through the SACs. |
abstractGer |
Aims: The transient receptor potential canonical channel 1 (TRPC1) is a crucial component of the stretch-activated ion channels (SACs). The objective of this research was to demonstrate the contribution of TRPC1 in maintaining cardiac contractile function in the hypertrophic myocardium. Methods: Hypertrophic rat hearts were induced by injecting isoproterenol intraperitoneally, and the expressions of TRPC1/3/6 and Na+/Ca2+ exchanger 1 (NCX1) proteins were analyzed by Western blot. The intracellular calcium images, the action potential of myocardium, the length-dependent contractile force of ventricle muscle and the cardiac output of isolated heart were investigated. Results: The expression of TRPC1 was increased in the hypertrophic myocardium. After being stretched, the ascendant amplitude of the increase in the intracellular calcium ion concentration ([Ca2+]i) in the hypertrophic myocardium was higher than that in the normal myocardium. The increase of the APD50 and the amplitude of the membrane potential depolarization were more significant in the hypertrophic myocardium after the activation of SACs. When the heart preparations were perfused with Tyrode's solution, there was no difference in the cardiac systolic function between the cardiac hypertrophy group and the control group. Gadolinium, a SACs blocker, reduced the length-dependent contractile force and suppressed the ascending limb of the Frank-Starling curves in the hypertrophic heart. Conclusions: The upregulation of TRPC1 contributes to the contractile function in the hypertrophic myocardium by increasing [Ca2+]i through the SACs. |
abstract_unstemmed |
Aims: The transient receptor potential canonical channel 1 (TRPC1) is a crucial component of the stretch-activated ion channels (SACs). The objective of this research was to demonstrate the contribution of TRPC1 in maintaining cardiac contractile function in the hypertrophic myocardium. Methods: Hypertrophic rat hearts were induced by injecting isoproterenol intraperitoneally, and the expressions of TRPC1/3/6 and Na+/Ca2+ exchanger 1 (NCX1) proteins were analyzed by Western blot. The intracellular calcium images, the action potential of myocardium, the length-dependent contractile force of ventricle muscle and the cardiac output of isolated heart were investigated. Results: The expression of TRPC1 was increased in the hypertrophic myocardium. After being stretched, the ascendant amplitude of the increase in the intracellular calcium ion concentration ([Ca2+]i) in the hypertrophic myocardium was higher than that in the normal myocardium. The increase of the APD50 and the amplitude of the membrane potential depolarization were more significant in the hypertrophic myocardium after the activation of SACs. When the heart preparations were perfused with Tyrode's solution, there was no difference in the cardiac systolic function between the cardiac hypertrophy group and the control group. Gadolinium, a SACs blocker, reduced the length-dependent contractile force and suppressed the ascending limb of the Frank-Starling curves in the hypertrophic heart. Conclusions: The upregulation of TRPC1 contributes to the contractile function in the hypertrophic myocardium by increasing [Ca2+]i through the SACs. |
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Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ023683996</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230501180308.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230226s2013 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1159/000354498</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ023683996</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ98ae924bab074131946028b713a9f814</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QP1-981</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QD415-436</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Mo-Si Chen</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2013</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Aims: The transient receptor potential canonical channel 1 (TRPC1) is a crucial component of the stretch-activated ion channels (SACs). The objective of this research was to demonstrate the contribution of TRPC1 in maintaining cardiac contractile function in the hypertrophic myocardium. Methods: Hypertrophic rat hearts were induced by injecting isoproterenol intraperitoneally, and the expressions of TRPC1/3/6 and Na+/Ca2+ exchanger 1 (NCX1) proteins were analyzed by Western blot. The intracellular calcium images, the action potential of myocardium, the length-dependent contractile force of ventricle muscle and the cardiac output of isolated heart were investigated. Results: The expression of TRPC1 was increased in the hypertrophic myocardium. After being stretched, the ascendant amplitude of the increase in the intracellular calcium ion concentration ([Ca2+]i) in the hypertrophic myocardium was higher than that in the normal myocardium. The increase of the APD50 and the amplitude of the membrane potential depolarization were more significant in the hypertrophic myocardium after the activation of SACs. When the heart preparations were perfused with Tyrode's solution, there was no difference in the cardiac systolic function between the cardiac hypertrophy group and the control group. Gadolinium, a SACs blocker, reduced the length-dependent contractile force and suppressed the ascending limb of the Frank-Starling curves in the hypertrophic heart. Conclusions: The upregulation of TRPC1 contributes to the contractile function in the hypertrophic myocardium by increasing [Ca2+]i through the SACs.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Transient receptor potential canonical channel 1</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Stretch-activated ion channels</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Hypertrophic myocardium</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Contractile function</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Physiology</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Biochemistry</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Jun-Hua Xiao</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yong Wang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Bo-Ming Xu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Lu Gao</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Jia-Ling Wang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Cellular Physiology and Biochemistry</subfield><subfield code="d">Cell Physiol Biochem Press GmbH & Co KG, 2002</subfield><subfield code="g">32(2013), 4, Seite 951-959</subfield><subfield code="w">(DE-627)300189702</subfield><subfield code="w">(DE-600)1482056-0</subfield><subfield code="x">14219778</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:32</subfield><subfield code="g">year:2013</subfield><subfield code="g">number:4</subfield><subfield code="g">pages:951-959</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1159/000354498</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/98ae924bab074131946028b713a9f814</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://www.karger.com/Article/FullText/354498</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1015-8987</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" 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