[Na+/H+ exchangers, alpha-2-adrenergic receptors, sodium sensitivity and arterial hypertension].
Existing evidences indicate that a crossed regulation between alpha 2-adrenergic receptors and Na+/H+ exchanger(s) exists, that Na decreases the affinity of alpha 2-adrenergic receptors for agonists and antagonists, that intracellular Na+ and H+ ion concentrations regulate Na+/H+ exchanger activity, that intracellular pH controls the affinity of the alpha 2-adrenergic receptors for their agonists and antagonists. Alterations of alpha 2-adrenergic receptor densities and allosteric regulation by sodium have been demonstrated in sodium-dependent hypertension in rats. Increased Na+/H+ exchanger activity has been reported in genetic hypertension. Nevertheless, cosegregation experiments and human genetic polymorphism suggest that the exchanger could not be related to hypertension. We propose the following hypothesis: the increased Na+/H+ exchanger characteristic of hypertension could be secondary to the abnormalities of the alpha 2-adrenergic receptors found in hypertension, probably through the alteration of the sodium allosteric effect on these receptors.
Cloix
J F
JF
Service de Biochimie de Paris-Ouest, UFR biomédicale des Saints-Pères, Paris.
Le Jossec
M
M
Baud
O
O
Pecquery
R
R
Giudicelli
Y
Y
Dausse
J P
JP
D000818:Animals; D004351:Drug Resistance; D006859:Hydrogen / Q000378:metabolism*; D006973:Hypertension / Q000209:etiology / Q000378:metabolism*; D017136:Ion Transport; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*; D012982:Sodium, Dietary / Q000009:adverse effects / Q000494:pharmacology*
D011942:Receptors, Adrenergic, alpha; D012982:Sodium, Dietary; D006859:Hydrogen; D012964:Sodium
Echangeurs Na+/H+, récepteurs alpha 2-adrénergiques, sensibilité au sodium et hypertension artérielle.