Pendrin as a regulator of ECF and blood pressure.
OBJECTIVE
Abnormal renal sodium handling plays a pivotal role in the pathophysiology of arterial hypertension. Though sodium is present in the diet as a chloride salt, most studies have focused on the renal mechanisms of sodium transport and their regulation, and very few have investigated the impact of chloride. However, strong evidence indicates that chloride may play a very important role in the 'prohypertensive' effects of sodium.


RESULTS
Several observations indicate that sodium has to be administered as NaCl and not as NaHCO3 to raise arterial blood pressure. Recently, genetic studies have pointed out the critical role of the most distal parts of the nephron in regulating sodium balance and blood pressure. Interestingly, in those segments, the transport of Na+ and Cl- proceeds separately, through different molecules. Recent evidence has demonstrated that an apical Cl-/HCO3- exchanger called pendrin is an absolute requirement for chloride reabsorption in the collecting system, indicating that chloride absorption is not passive and paracellular but is mediated by the intercalated cells. Importantly, pendrin disruption protects mice against mineralocorticoid-induced hypertension and impairs renal adaptation to a low NaCl diet. Moreover, recent findings suggest several mechanisms by which chloride transport might affect NaCl balance and blood pressure.


CONCLUSIONS
Pendrin-mediated chloride transport through intercalated cells appears to be an independent and important determinant of renal NaCl handling and therefore might represent a new target for blood pressure control.
Eladari
Dominique
D
Centre de recherche des Cordeliers, INSERM U 872 (equipe 3), ERL CNRS 7226, Paris, France. dominique.eladari@crc.jussieu.fr
Chambrey
Régine
R
Frische
Sebastian
S
Vallet
Marion
M
Edwards
Aurélie
A
D000818:Animals; D001794:Blood Pressure; D027963:Chloride-Bicarbonate Antiporters / Q000502:physiology; D002712:Chlorides / Q000378:metabolism*; D045604:Extracellular Fluid / Q000378:metabolism*; D006801:Humans; D017136:Ion Transport; D007668:Kidney / Q000378:metabolism; D007686:Kidney Tubules, Distal / Q000378:metabolism; D026901:Membrane Transport Proteins / Q000502:physiology*; D009399:Nephrons / Q000378:metabolism; D012965:Sodium Chloride / Q000378:metabolism; D000076988:Sulfate Transporters
D027963:Chloride-Bicarbonate Antiporters; D002712:Chlorides; D026901:Membrane Transport Proteins; C085609:SLC26A4 protein, human; D000076988:Sulfate Transporters; D012965:Sodium Chloride