[Na+, K+, Cl-]-cotransport function and dysfunction in different forms of primary hypertension.
We investigated the effect of an increase in cell Na+ content on outward and inward unidirectional fluxes catalyzed by the [Na+, K+, Cl-]-cotransport system in human erythrocytes (incubated in Li-Rb media). Erythrocytes with low Na+ content exhibited an uncoupled K+ efflux. The increase in cell Na+ content resulted in a more marked stimulation of outward Na+, K+ than of inward Li+, Rb+ cotransport fluxes (with stoichiometries not very different from one-to-one). These results suggest that in human erythrocytes and in nonepithelial cells with small but outwardly directed electrochemical Cl- gradients, the [Na+, K+, Cl-]-cotransport system may behave as a "second pump" by using the extra energy supplied by an additional net [K+, Cl-] efflux. The [Na+, K+, Cl-]-cotransport system (of vascular cells and/or noradrenergic endings) may play two different roles in primary hypertension: (a) "defective second pump" in some essential hypertensive patients with decreased cotransport affinity for internal Na+ and (b) "compensatory second pump" in other forms of primary hypertension where abnormalities in the Na+, K+ pump or in other ion transport systems may predispose the cell to a defective extrusion of excess cell Na+ content.
INSERM U7/CNRS LA 318, Hôpital Necker, Paris, France.
M N
MN
Saitta
P A
PA
Hannaert
C
C
Rosati
A S
AS
Diaz
N
N
Senn
R P
RP
Garay
D001692:Biological Transport; D002352:Carrier Proteins / Q000502:physiology*; D055598:Chemical Phenomena; D002621:Chemistry; D004912:Erythrocytes / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008094:Lithium / Q000097:blood; D008433:Mathematics; D012413:Rubidium / Q000097:blood; D012964:Sodium / Q000097:blood; D028021:Sodium-Potassium-Chloride Symporters
D002352:Carrier Proteins; D028021:Sodium-Potassium-Chloride Symporters; D008094:Lithium; D012964:Sodium; D012413:Rubidium