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Günter A.J. Riegger

Researcher at University of Regensburg

Publications -  199
Citations -  8882

Günter A.J. Riegger is an academic researcher from University of Regensburg. The author has contributed to research in topics: Heart failure & Renin–angiotensin system. The author has an hindex of 52, co-authored 199 publications receiving 8570 citations.

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Association between a deletion polymorphism of the angiotensin-converting-enzyme gene and left ventricular hypertrophy.

TL;DR: The findings suggest thatleft ventricular hypertrophy is partially determined by genetic disposition and identifies the DD genotype of ACE as a potential genetic marker associated with an elevated risk of left ventricularhypertrophy in middle-aged men.
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A comprehensive linkage analysis for myocardial infarction and its related risk factors.

TL;DR: It is shown, by using variance component analysis and incorporating risk factors, that risk of myocardial infarction maps to a single region on chromosome 14 with a significant lod score of 3.9, providing evidence of a principal MI locus.
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Determinants of interindividual variation of renin and prorenin concentrations: evidence for a sexual dimorphism of (pro)renin levels in humans.

TL;DR: There is a sexual dimorphism of prorenin levels in humans, suggesting that sex hormones affect the regulation of the renin gene, and data confirm previous reports of elevated prorenIn levels in diabetics and older subjects, as well as of lower than normal levels in subjects with hypertension in smaller populations.
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Development of heart failure following isoproterenol administration in the rat: role of the renin–angiotensin system

TL;DR: In rats, a toxic dosage of isoproterenol caused characteristic myocardial damage that subsequently resulted in mild heart failure that seems to require functional integrity of the renin-angiotensin system.
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Angiotensin II-induced growth responses in isolated adult rat hearts. Evidence for load-independent induction of cardiac protein synthesis by angiotensin II.

TL;DR: Compared with phorbol ester stimulation, angiotensin II effects on PKC translocation were significantly less pronounced and required a more prolonged stimulation, and the pathways of angiotsin signal transduction, protein kinase C (PKC)-epsilon as well as cardiac c-fos and c-jun mRNA levels were analyzed.