1166 A/C polymorphism of the angiotensin II type 1 receptor gene and the response to short-term infusion of angiotensin II | |
Article | |
关键词: HUMAN ESSENTIAL-HYPERTENSION; CONVERTING ENZYME GENE; MYOCARDIAL-INFARCTION; DELETION POLYMORPHISM; A/C-1166 POLYMORPHISM; BLOOD-PRESSURE; RISK FACTOR; ASSOCIATION; LINKAGE; SYSTEM; | |
DOI : 10.1161/01.CIR.100.13.1394 | |
来源: SCIE |
【 摘 要 】
Background-Previous 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 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 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. 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 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.
【 授权许可】
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