Title

Regulation of prostasin by aldosterone in the kidney

Authors

Authors

T. Narikiyo; K. Kitamura; M. Adachi; T. Miyoshi; K. Iwashita; N. Shiraishi; H. Nonoguchi; L. M. Chen; K. X. Chai; J. Chao;K. Tomita

Comments

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Abbreviated Journal Title

J. Clin. Invest.

Keywords

EPITHELIAL SODIUM-CHANNEL; CORTICAL COLLECTING DUCT; K+; TRANSPORT-PROPERTIES; NAFAMOSTAT MESILATE; INDUCED PROTEIN; LOCALIZATION; HYPERKALEMIA; EXPRESSION; ACTIVATION; SUBUNIT; Medicine, Research & Experimental

Abstract

Prostasin is a serine protease present in mammalian urine that increases the activity of the epithelial sodium channel (ENaC) when the two are coexpressed in Xenopus oocytes. To determine if aldosterone, one of the principal regulators of urinary Na reabsorption by the distal nephron, affects prostasin expression, we examined prostasin mRNA and protein in a cultured mouse cortical collecting duct cell line (M-1), whole rats, and patients with primary aldosteronism. Aldosterone treatment of M-1 cells substantially increased prostasin expression and stimulated Na-22 uptake. Urinary excretion of prostasin in rats that were infused with aldosterone likwise increased by similar to4-fold when compared with the vehicle-infused rats. Finally, urinary excretion of prostasin in patients with primary aldosteronism was substantially increased when compared with normal patients. Adrenalectomy reduced urinary prostasin excretion to control levels, whereas urinary prostasin levels were not altered in patients undergoing surgery, for other reasons. In patients with primary aldosteronism, reduction in the urinary excretion of prostasin correlated with the increase in the urinary Na/K ratio. These Findings, together with our previous report that prostasin activates the amiloride-sensitive Na currents through ENaC, demonstrate that prostasin regulates Na balance in vivo by virtue of its heightened expression in the presence of aldosterone.

Journal Title

Journal of Clinical Investigation

Volume

109

Issue/Number

3

Publication Date

1-1-2002

Document Type

Article

Language

English

First Page

401

Last Page

408

WOS Identifier

WOS:000173710500015

ISSN

0021-9738

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