[Na-K-Cl cotransporters and "salt-sensitive" arterial hypertension].
In the 80s, erythrocyte Na-K-Cl cotransporter of essential hypertensive was reported: (i) decreased in fresh erythrocytes and (ii) increased, following repeated cell washings and incubations. This suggested to us that the manipulation of erythrocytes (from essential hypertensives) was able to dissociate a cotransport inhibitory factor, thus unmasking up-regulation of membrane cotransport units. This working hypothesis was recently confirmed in Dahl salt-sensitive rats (DS). The primary defect of DS rats seems to be hyperactivity of cotransporter Na-K-Cl BSC1 at the thick ascending limb of Henle's loop (TAL). Moreover, oral salt-loading induces an abnormally high increase in the urinary and plasmatic CIF levels of DS rats. The increase in urinary CIF excretion seems to be a compensatory mechanism, able to reduce BSC1 hyperactivity and NaCl reabsorption at the TAL. The increase in plasmatic CIF should inhibit erythrocyte BSC2, thus inducing "up-regulation" of the membrane density of cotransport proteins. Further studies are required to test this model in human with "salt-sensitive" hypertension.
Garay
R P
RP
INSERM U400, faculté de médecine de Créteil.
Alvarez-Guerra
M
M
D000042:Absorption; D000284:Administration, Oral; D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism*; D004912:Erythrocytes / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000209:etiology; D051381:Rats; D020303:Rats, Inbred Dahl; D012965:Sodium Chloride / Q000009:adverse effects* / Q000493:pharmacokinetics; D028021:Sodium-Potassium-Chloride Symporters
D002352:Carrier Proteins; D028021:Sodium-Potassium-Chloride Symporters; D012965:Sodium Chloride