(Circulation. 1999;100:1394-1399.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Department of Medicine/Nephrology, University of Erlangen-Nürnberg, Germany.
Correspondence to Prof Dr Roland E. Schmieder, Medizinische Klinik IV der Universität Erlangen-Nürnberg, Breslauer Strasse 201, D-90471 Nürnberg, Germany.
BackgroundPrevious studies reported an association of the 1166 A/C polymorphism of the angiotensin II (Ang II) type 1 receptor gene with high blood pressure and cardiovascular disease. We tested the hypothesis that this polymorphism affects the blood-pressure, renal hemodynamic, and aldosterone response to infused Ang II.
Methods and ResultsYoung, male, white volunteers (n=116) with normal (n=65) or mildly elevated (n=51) blood pressure on a high salt intake were genotyped for the 1166 A/C polymorphism. Two doses of Ang II (0.5 and 3 ng · kg-1 · min-1 over 30 minutes each) increased blood pressure, plasma aldosterone, glomerular filtration rate, and filtration fraction and decreased renal blood flow. The blood-pressure, renal hemodynamic, and aldosterone responses were not significantly different between subjects homozygous for the A allele (n=56) and heterozygous subjects (n=47) or subjects homozygous for the C allele (n=13). Comparison of A allele homozygotes with all C allele carriers pooled (n=60) or restriction of the analysis to normotensive volunteers also revealed no significant differences between genotypes.
ConclusionsThe 1166 C variant of the Ang II type 1 receptor does not lead to a greater blood-pressure, aldosterone, or renal vascular response to infused Ang II in young, male, white subjects. We conclude that the 1166 A/C polymorphism does not have a major effect on these actions of Ang II.
Key Words: angiotensin genes kidney blood pressure
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