| First Author | Cheval L | Year | 2019 |
| Journal | Am J Physiol Renal Physiol | Volume | 317 |
| Issue | 2 | Pages | F435-F443 |
| PubMed ID | 31188029 | Mgi Jnum | J:284445 |
| Mgi Id | MGI:6381216 | Doi | 10.1152/ajprenal.00059.2019 |
| Citation | Cheval L, et al. (2019) ANP-stimulated Na(+) secretion in the collecting duct prevents Na(+) retention in the renal adaptation to acid load. Am J Physiol Renal Physiol 317(2):F435-F443 |
| abstractText | 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 NH4Cl-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. |
