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Association between markers in chromosomal region 17q23 and young onset hypertension: a TDT study
  1. S-Y Wu1,2,
  2. C S J Fann2,
  3. Y-S Jou3,
  4. J-W Chen4,
  5. W-H Pan2
  1. 1Graduate Institute of Life Sciences, National Defence Medical Centre, Taipei, Taiwan
  2. 2Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
  3. 3Division of Molecular and Genomic Medicine, National Health Research Institutes, Taipei, Taiwan
  4. 4Department of Cardiology, Taipei Veterans General Hospital, and Cardiovascular Research Centre, National Yang-Ming University, Taipei, Taiwan
  1. Correspondence to:
 Dr W-H Pan, Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan;

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Hypertension is one of the most important risk factors for cardiovascular diseases. Despite extensive research examining the causes of blood pressure variation, a significant proportion of blood pressure variation is yet to be explained. Studies of families and twins suggest that 20-40% of blood pressure variation can be attributed to genetic factors.1 Evidence shows that the genetic contribution is even greater for young onset hypertension.2 We feel that genetic approaches focusing on young onset hypertension will provide new insight into the pathogenesis of hypertension.

In our previous report, the affected sib pairs (25 independent, affected sib pairs) method showed positive signs of linkage for markers of the atrial natriuretic peptide gene (NPPA) (D1S1612, p=0.0162), angiotensinogen gene (AGT) (D1S547, p=0.0263), lipoprotein lipase gene (LPL) (D8S1145, p=0.0284), and angiotensin converting enzyme gene (DCP1) (D17S2193, p=0.0256),3 indicating that multiple pathogenic pathways may be involved in the aetiology of young onset hypertension. Owing to this aetiological complexity, in the current study we focus on high resolution mapping of AGT (located on 1q42-43) and DCP1 (located on 17q23), genes of the renin angiotensin system (RAS). Renin catalyses the first step of the activation pathway of angiotensinogen to angiotensin I, which is then cleaved to angiotensin II by angiotensin I converting enzyme. This cascade can lead to aldosterone release, vasoconstriction, and increased blood pressure. Although the RAS has been extensively studied, it remains unclear how and to what extent RAS gene variants contribute to the blood pressure variations in various human populations.


We have recruited 59 nuclear families (a total of 214 subjects) from a hypertension clinic at Taipei …

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