Effects of angiotensin II on kinase-mediated sodium and potassium transport in the distal nephron

Nils Lubbe, R. Zietse, Ewout Hoorn

Research output: Contribution to journalArticleAcademicpeer-review

28 Citations (Scopus)

Abstract

Purpose of review The aim is to review the recently reported effects of angiotensin II (Ang II) on sodium and potassium transport in the aldosterone-sensitive distal nephron, including the signaling pathways between receptor and transporter, and the (patho)physiological implications of these findings. Recent findings Ang II can activate the sodium chloride cotransporter (NCC) through phosphorylation by Ste20-related, proline-alanine rich kinase (SPAK), an effect that is independent of aldosterone but dependent on with no lysine kinase 4 (WNK4). A low-sodium diet (high Ang II) activates NCC, whereas a high-potassium diet (low Ang II) inhibits NCC. NCC activation also contributes to Ang-II-mediated hypertension. Ang II also activates the epithelial sodium channel (ENaC) additively to aldosterone, and this effe Summary The effects of Ang II on NCC, ENaC, and ROMK help explain the renal response to hypovolemia which is to conserve both sodium and potassium. Pathophysiologically, Ang-II-induced activation of NCC appears to contribute to salt-sensitive hypertension.
Original languageUndefined/Unknown
Pages (from-to)120-126
Number of pages7
JournalCurrent Opinion in Nephrology and Hypertension
Volume22
Issue number1
DOIs
Publication statusPublished - 2013

Cite this