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

Gespeichert in:

Autor*in:	Mo-Si Chen [verfasserIn] Jun-Hua Xiao [verfasserIn] Yong Wang [verfasserIn] Bo-Ming Xu [verfasserIn] Lu Gao [verfasserIn] Jia-Ling Wang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2013

Schlagwörter:	Transient receptor potential canonical channel 1 Stretch-activated ion channels Hypertrophic myocardium Contractile function

Übergeordnetes Werk:	In: Cellular Physiology and Biochemistry - Cell Physiol Biochem Press GmbH & Co KG, 2002, 32(2013), 4, Seite 951-959
Übergeordnetes Werk:	volume:32 ; year:2013 ; number:4 ; pages:951-959

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1159/000354498

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.
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allfields	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
spelling	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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callnumber-first	Q - Science
author	Mo-Si Chen
spellingShingle	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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topic_title	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
topic	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
topic_unstemmed	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
topic_browse	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
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title	Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat
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title_full	Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat
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author_browse	Mo-Si Chen Jun-Hua Xiao Yong Wang Bo-Ming Xu Lu Gao Jia-Ling Wang
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title_sort	upregulation of trpc1 contributes to contractile function in isoproterenol-induced hypertrophic myocardium of rat
callnumber	QP1-981
title_auth	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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title_short	Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat
url	https://doi.org/10.1159/000354498 https://doaj.org/article/98ae924bab074131946028b713a9f814 http://www.karger.com/Article/FullText/354498 https://doaj.org/toc/1015-8987 https://doaj.org/toc/1421-9778
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up_date	2024-07-03T18:56:01.445Z
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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. 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Upregulation of TRPC1 Contributes to Contractile Function in Isoproterenol-induced Hypertrophic Myocardium of Rat

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