Polymorphisms of EDNRB, ATG, and ACE genes in salt-sensitive hypertension

Jessica Caprioli, Caterina Mele, Chiara Mossali, Laura Gallizioli, Gilberta Giacchetti, Marina Noris, Giuseppe Remuzzi, Ariela Benigni

Research output: Contribution to journalArticlepeer-review


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 (ETBR)-deficient rats develop salt-sensitive hypertension when fed a high-salt diet. Whether the ETBR 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 ACEDD/ID genotypes. In conclusion, our data confirm the role of ET system and RAAS in salt-sensitive hypertension.

Original languageEnglish
Pages (from-to)505-510
Number of pages6
JournalCanadian Journal of Physiology and Pharmacology
Issue number8
Publication statusPublished - Aug 2008


  • Endothelin system
  • Polymorphism
  • Renin-angiotensin-aldosterone system
  • Salt-sensitive hypertension

ASJC Scopus subject areas

  • Physiology
  • Pharmacology


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