Association of M235T variant of the angiotensinogen gene with familial hypertension of early onset

Item Type:	Article
Title:	Association of M235T variant of the angiotensinogen gene with familial hypertension of early onset
Creators Name:	Schmidt, S. and Sharma, A.M. and Zilch, O. and Beige, J. and Walla-Friedel, M. and Ganten, D. and Distler, A. and Ritz, E.
Abstract:	A higher frequency of a variant of the angiotensinogen gene characterized by a transition in exon 2 causing a replacement of methionine by threonine (M235T) has recently been found in hypertensive individuals, but not all authors were able to confirm this observation. We examined (i) 219 patients with primary hypertension, (ii) 92 normotensive controls (spouses), and (iii) a sample of the general population (blood donors, n = 139). Analysis of genomic DNA was performed by PCR amplification and alleles were separated on agarose gels. In the general population and in normotensive spouses the respective frequencies of the T and M alleles were: general population: M = 0.6, T = 0.4; normotensive spouses: M = 0.59, T = 0.41. A significantly higher frequency of the 235T allele was found in hypertensive individuals with a family history of hypertension and an onset of hypertension before 50 years of age (spouses: 0.41 versus HT with age of onset < or = 50 years and family history of HT: 0.56; P = 0.01 by chi 2). In conclusion, the present study confirms the observation of a higher frequency of the 235T allele of the angiotensinogen gene in hypertension and identifies individuals with family history and early onset of hypertension as individuals at risk.
Keywords:	Alleles, Angiotensinogen, Base Sequence, Genotype, Hypertension, Medical Records, Molecular Probes, Molecular Sequence Data, Genetic Polymorphism
Source:	Nephrology Dialysis Transplantation
ISSN:	0931-0509
Publisher:	Oxford University Press
Volume:	10
Number:	7
Page Range:	1145-1148
Date:	1995
Official Publication:	http://ndt.oxfordjournals.org/content/10/7/1145.abstract
PubMed:	View item in PubMed

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