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

Cheval, Lydie; Bakouh, Naziha; Walter, Christine; Tembely, Dignê; Morla, Luciana; Escher, Geneviève; Vogt, Bruno; Crambert, Gilles; Planelles, Gabrielle; Doucet, Alain (2019). ANP-stimulated Na+ secretion in the collecting duct prevents Na+ retention in the renal adaptation to acid load. American journal of physiology. Renal physiology, 317(2), F435-F443. American Physiological Society 10.1152/ajprenal.00059.2019

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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 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.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Dermatology, Urology, Rheumatology, Nephrology, Osteoporosis (DURN) > Clinic of Nephrology and Hypertension

UniBE Contributor:

Escher, Geneviève

Subjects:

600 Technology > 610 Medicine & health
500 Science > 570 Life sciences; biology

ISSN:

1522-1466

Publisher:

American Physiological Society

Language:

English

Submitter:

Geneviève Escher

Date Deposited:

02 Sep 2019 14:16

Last Modified:

25 Oct 2019 16:29

Publisher DOI:

10.1152/ajprenal.00059.2019

PubMed ID:

31188029

Uncontrolled Keywords:

H-K-ATPase aldosterone atrial natriuretic peptide cGMP collecting duct metabolic acidosis sodium secretion

BORIS DOI:

10.7892/boris.132825

URI:

https://boris.unibe.ch/id/eprint/132825

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