Polymorphisms of<i>EDNRB</i>,<i>ATG</i>, and<i>ACE</i>genes in salt-sensitive hypertensionThis article is one of a selection of papers published in the special issue (part 2 of 2) on Forefronts in Endothelin.

DOI Web Site Web Site 被引用文献1件
  • Jessica Caprioli
    Clinical Research Center for Rare Diseases (Aldo e Cele Daccò), Mario Negri Institute for Pharmacological Research, Via Camozzi 3, 24020 Ranica, Bergamo, Italy.
  • Caterina Mele
    Clinical Research Center for Rare Diseases (Aldo e Cele Daccò), Mario Negri Institute for Pharmacological Research, Via Camozzi 3, 24020 Ranica, Bergamo, Italy.
  • Chiara Mossali
    Clinical Research Center for Rare Diseases (Aldo e Cele Daccò), Mario Negri Institute for Pharmacological Research, Via Camozzi 3, 24020 Ranica, Bergamo, Italy.
  • Laura Gallizioli
    Clinical Research Center for Rare Diseases (Aldo e Cele Daccò), Mario Negri Institute for Pharmacological Research, Via Camozzi 3, 24020 Ranica, Bergamo, Italy.
  • Gilberta Giacchetti
    Clinical Research Center for Rare Diseases (Aldo e Cele Daccò), Mario Negri Institute for Pharmacological Research, Via Camozzi 3, 24020 Ranica, Bergamo, Italy.
  • Marina Noris
    Clinical Research Center for Rare Diseases (Aldo e Cele Daccò), Mario Negri Institute for Pharmacological Research, Via Camozzi 3, 24020 Ranica, Bergamo, Italy.
  • Giuseppe Remuzzi
    Clinical Research Center for Rare Diseases (Aldo e Cele Daccò), Mario Negri Institute for Pharmacological Research, Via Camozzi 3, 24020 Ranica, Bergamo, Italy.
  • Ariela Benigni
    Clinical Research Center for Rare Diseases (Aldo e Cele Daccò), Mario Negri Institute for Pharmacological Research, Via Camozzi 3, 24020 Ranica, Bergamo, Italy.

書誌事項

公開日
2008-08
権利情報
  • http://www.nrcresearchpress.com/page/about/CorporateTextAndDataMining
DOI
  • 10.1139/y08-045
公開者
Canadian Science Publishing

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説明

<jats:p>Almost 50% of hypertensive individuals manifest blood pressure changes in response to salt depletion or repletion and are termed “salt sensitive” (SS). Blunted activity of the endothelin (ET) system and the renin–angiotensin–aldosterone system (RAAS) have been reported as possible mechanisms contributing to salt sensitivity. Data are available that endothelin receptor subtype B (ET<jats:sub>B</jats:sub>R)-deficient rats develop salt-sensitive hypertension when fed a high-salt diet. Whether the ET<jats:sub>B</jats:sub>R gene (EDNRB) is involved in genetic predisposition to human salt-sensitive hypertension has not been studied so far. We screened EDNRB in 104 hypertensive patients (49 salt sensitive and 55 salt resistant) and 110 normotensive controls. No new sequence variation was found, but genotype distribution of the common polymorphism G1065A revealed that the AA + GA genotypes were significantly more frequent in salt-resistant than in salt-sensitive individuals (p = 0.007), suggesting a protective role for the A allele. We also screened angiotensinogen gene AGT M235T and angiotensin-converting enzyme insertion/deletion polymorphism ACE I/D and found an association between TT genotype and hypertension. A possible synergistic effect to salt-sensitive hypertension was found by combining EDNRB GG with ACE DD/ID genotypes. In conclusion, our data confirm the role of ET system and RAAS in salt-sensitive hypertension.</jats:p>

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