Angiotensin II induziert Nox 2 -abhängig Arrhythmien in ventrikulären Kardiomyozyten der Maus

Azizian, Azadeh

dc.contributor.advisor	Maier, Lars S. Prof. Dr.
dc.contributor.author	Azizian, Azadeh
dc.date.accessioned	2015-10-28T07:07:08Z
dc.date.available	2015-11-04T23:50:05Z
dc.date.issued	2015-10-28
dc.identifier.uri	http://hdl.handle.net/11858/00-1735-0000-0023-965F-2
dc.identifier.uri	http://dx.doi.org/10.53846/goediss-5335
dc.identifier.uri	http://dx.doi.org/10.53846/goediss-5335
dc.language.iso	deu	de
dc.rights.uri	http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.ddc	610	de
dc.title	Angiotensin II induziert Nox 2 -abhängig Arrhythmien in ventrikulären Kardiomyozyten der Maus	de
dc.type	doctoralThesis	de
dc.title.translated	Angiotensin II induces Nox 2- dependent arrhythmias in ventricular cardiomyocytes of mice	de
dc.contributor.referee	Lutz, Susanne Prof. Dr.
dc.date.examination	2015-10-28
dc.description.abstracteng	Heart failure and cardiac arrhythmias are prevalent diseases which occure mainly in older patients. With regard to the demographic change their importance will even increase in the nexts decades. Mechanisms of heart failure and the developement of arrhythmia are not fully understood yet. The aim of this study is to analyze the role of angiotensin II, NADPH-Oxidase II (Nox2) and CaMKII in this context. Therefore we used two mouse models: CaMKIIδ-Knockout-Mice and gp91phox-Knockout-Mice, both were compared to their wild type. In isolated cardiomyocytes of these mice, we measured action potentials using patch-clamp-technic in whole-cell-configuration and current-clamp-mode. The measurements were performed a) without any pharmacologic intervention b) by adding angiotensin II and c) by adding angiotensin II and DPI (a Nox-2-inhibitor). Our results show that angiotensin increases peak Na current during the action potential. This effect was absent in myocytes lacking functional Nox2 (gp91phox(-/-)). In contrast, genetic knockout of CaMKIIδ (CaMKIIδ(-/-)) did not influence the Ang II-dependent increase in peak INa. Furthermore the results show that Ang II increased the propensity for cellular arrhythmias, for which CaMKII contributes, dependent on Nox2.	de
dc.contributor.coReferee	Schön, Margarete Prof. Dr.
dc.subject.ger	Angiotensin II	de
dc.subject.ger	CaMKII	de
dc.subject.ger	NADPH-Oxidase II	de
dc.subject.ger	Arrhythmien	de
dc.subject.ger	Kardiomyozyten	de
dc.subject.eng	Angiotensin II	de
dc.subject.eng	Arrhythmia	de
dc.subject.eng	Nadph-oxidase II	de
dc.subject.eng	CaMKII	de
dc.identifier.urn	urn:nbn:de:gbv:7-11858/00-1735-0000-0023-965F-2-9
dc.affiliation.institute	Medizinische Fakultät	de
dc.subject.gokfull	Medizin (PPN619874732)	de
dc.description.embargoed	2015-11-04
dc.identifier.ppn	837983290

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Human- und Zahnmedizin [2872]

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