Na+/H+ exchangers, alpha-2-adrenergic receptors, sodium sensitivity and arterial hypertension
Cloix, J.F.; Le Jossec, M.; Baud, O.; Pecquery, R.; Giudicelli, Y.; Dausse, J.P.
Comptes Rendus des Seances de la Societe de Biologie et de ses Filiales 186(4): 377-386
1992
ISSN/ISBN: 0037-9026 PMID: 1338697 Document Number: 400441
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.