Abstract

Na(+) is commonly designed as the culprit of salt-sensitive hypertension but several studies suggest that abnormal Cl(-) transport is in fact the triggering mechanism. This review focuses on the regulation of blood pressure (BP) by pendrin, an apical Cl(-)/HCO(3)(-) exchanger which mediates HCO(3)(-) secretion and transcellular Cl(-) transport in type B intercalated cells (B-ICs) of the distal nephron. Studies in mice showed that it is required not only for acid-base regulation but also for BP regulation as pendrin knock-out mice develop hypotension when submitted to NaCl restriction and are resistant to aldosterone-induced hypertension. Pendrin contributes to these processes by two mechanisms. First, pendrin-mediated Cl(-) transport is coupled with Na(+) reabsorption by the Na(+)-dependent Cl(-)/HCO(3)(-) exchanger NDCBE to mediate NaCl reabsorption in B-ICs. Second, pendrin activity regulates Na(+) reabsorption by the adjacent principal cells, possibly by interaction with the ATP-mediated paracrine signalling recently identified between ICs and principal cells. Interestingly, the water channel AQP5 was recently found to be expressed at the apical side of B-ICs, in the absence of a basolateral water channel, and pendrin and AQP5 membrane expressions are both inhibited by K(+) depletion, suggesting that pendrin and AQP5 could cooperate to regulate cell volume, a potent stimulus of ATP release.

Autore Pugliese

• Valenti Giovanna , Procino Giuseppe

Tutti gli autori

• VALENTI G.;PROCINO G.

Titolo volume/Rivista

Non Disponibile

Anno di pubblicazione

2011

ISSN

1015-8987

ISBN

Non Disponibile

Numero di citazioni Wos

Nessuna citazione

Ultimo Aggiornamento Citazioni

Non Disponibile

Numero di citazioni Scopus

17

Ultimo Aggiornamento Citazioni

Non Disponibile

Settori ERC

Non Disponibile

Codici ASJC

Non Disponibile