1166 A/C polymorphism of the angiotensin II type 1 receptor gene and the response to short-term infusion of angiotensin II

Citation
Kf. Hilgers et al., 1166 A/C polymorphism of the angiotensin II type 1 receptor gene and the response to short-term infusion of angiotensin II, CIRCULATION, 100(13), 1999, pp. 1394-1399
Citations number
34
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CIRCULATION
ISSN journal
00097322 → ACNP
Volume
100
Issue
13
Year of publication
1999
Pages
1394 - 1399
Database
ISI
SICI code
0009-7322(19990928)100:13<1394:1APOTA>2.0.ZU;2-M
Abstract
Background-Previous studies reported an association of the 1166 A/C polymor phism of the angiotensin II (Ang II) type 1 receptor gene with high blood p ressure and cardiovascular disease. We tested the hypothesis that this poly morphism affects the blood-pressure, renal hemodynamic, and aldosterone res ponse to infused Ang II. Methods and Results-Young, 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 aldo sterone, glomerular filtration rate, and filtration fraction and decreased renal blood flow. The blood-pressure, renal hemodynamic, and aldosterone re sponses were not significantly different between subjects homozygous for th e A allele (n = 56) and heterozygous subjects (n = 47) or subjects homozygo us 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 normoten sive volunteers also revealed no significant differences between genotypes. Conclusions-The 1166 C variant of the Ang II type I receptor does not lead to a greater blood-pressure, aldosterone, or renal vascular response to inf used Ang II in young, male, white subjects. We conclude that the 1166 A/C p olymorphism does not have a major effect on these actions of Ang II.