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We have recently reported that type A intercalated cells of the collecting duct secrete Na +  by a mechanism coupling the basolateral type 1 Na + -K + -2Cl −  cotransporter with apical type 2 H + -K + -ATPase (HKA2) functioning under its Na + /K +  exchange mode. The first aim of the present study was to evaluate whether this secretory pathway is a target of atrial natriuretic peptide (ANP). Despite hyperaldosteronemia, metabolic acidosis is not associated with Na +  retention. The second aim of the present study was to evaluate whether ANP-induced stimulation of Na +  secretion by type A intercalated cells might account for mineralocorticoid escape during metabolic acidosis. In Xenopus oocytes expressing HKA2, cGMP, the second messenger of ANP, increased the membrane expression, activity, and Na + -transporting rate of HKA2. Feeding mice with a NH 4 Cl-enriched diet increased urinary excretion of aldosterone and induced a transient Na +  retention that reversed within 3 days. At that time, expression of ANP mRNA in the collecting duct and urinary excretion of cGMP were increased. Reversion of Na +  retention was prevented by treatment with an inhibitor of ANP receptors and was absent in HKA2-null mice. In conclusion, paracrine stimulation of HKA2 by ANP is responsible for the escape of the Na + -retaining effect of aldosterone during metabolic acidosis.

ANP-stimulated Na+ secretion in the collecting duct prevents Na+ retention in the renal adaptation to acid load

ANP-stimulated Na⁺ secretion in the collecting duct prevents Na⁺ retention in the renal adaptation to acid load