4.2 Article

Lack of association between polymorphisms in STK39, a putative thiazide response gene, and blood pressure response to hydrochlorothiazide

Journal

PHARMACOGENETICS AND GENOMICS
Volume 20, Issue 8, Pages 516-519

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/FPC.0b013e32833b5958

Keywords

blood pressure; diuretics; hydrochlorothiazide; hypertension; pharmacogenetics; single nucleotide polymorphisms; ste20/SPS1-related proline/alanine-rich kinase; STK39; thiazides

Funding

  1. NIH [HL 74735, HL 53335, U01 GM074492, M01 RR00082, UL1 RR029890, UL1 RR025008, M01 RR00039, UL1 RR024150, T32 DK007518]
  2. Mayo Foundation

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STK39 was earlier implicated as a hypertension susceptibility gene and is thought to be involved in the control of Na(+)-Cl(-) co-transporter activity. STK39 has been implicated as a putative thiazide diuretic response gene, as Na(+)-Cl(-) co-transporter activity is inhibited by thiazides. Thus, we aimed to determine whether STK39 is a thiazide response gene. One hundred and ninety-five 'good' and 194 'poor' responders to hydrochlorothiazide (HCTZ) were genotyped for approximately 100 single nucleotide polymorphisms (SNPs) within 5000 bases of STK39. SNPs meeting criteria for advancement to replication analysis (P<0.01), along with those earlier associated with hypertension, were then analyzed in a second population of 201 HCTZ-treated hypertensives. Two SNPs passed screening and were further analyzed. However, neither these, nor earlier implicated SNPs met criteria for significant association with blood pressure response to HCTZ. These data suggest that common variants in STK39 likely do not have a clinically relevant role in blood pressure response to HCTZ in hypertensives. Pharmacogenetics and Genomics 20: 516-519 (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

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