Direct activation of ENaC by angiotensin II: Recent advances and new insights

Oleg Zaika, Mykola Mamenko, Alexander Staruschenko, Oleh Pochynyuk

Research output: Contribution to journalReview articlepeer-review

53 Scopus citations


Angiotensin II (Ang II) is the principal effector of the renin-angiotensin-aldosterone system (RAAS). It initiates myriad processes in multiple organs integrated to increase circulating volume and elevate systemic blood pressure. In the kidney, Ang II stimulates renal tubular water and salt reabsorption causing antinatriuresis and antidiuresis. Activation of the RAAS is known to enhance activity of the epithelial Na+ channel (ENaC) in the aldosterone-sensitive distal nephron. In addition to its well described stimulatory actions on aldosterone secretion, Ang II is also capable of directly increasing ENaC activity. In this brief review, we discuss recent findings about non-classical Ang II actions on ENaC and speculate about its relevance for renal sodium handling.

Original languageEnglish (US)
Pages (from-to)17-24
Number of pages8
JournalCurrent Hypertension Reports
Issue number1
StatePublished - Feb 2013
Externally publishedYes


  • AT receptors
  • Aldosterone
  • Aldosterone paradox
  • Aldosterone-sensitive distal nephron
  • Collecting duct, Connected tubule, Mineralocorticoid receptors
  • Hypertension
  • Intrarenal RAS
  • RAAS
  • Renin-angiotensin-aldosterone system
  • Salt-sensitive hypertension
  • Sodium reabsorption

ASJC Scopus subject areas

  • Internal Medicine


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