Hormonal regulation of the epithelial Na+ channel:: From amphibians to mammals

被引：29

作者：

Shane, Michael Anne ^{[1
]}

Nofziger, Charity ^{[1
]}

Blazer-Yost, Bonnie L. ^{[1
]}

机构：

[1] Purdue Univ, Dept Biol, Indianapolis, IN USA

来源：

GENERAL AND COMPARATIVE ENDOCRINOLOGY | 2006年 / 147卷 / 01期

关键词：

aldosterone; insulin; vasopressin; vasotocin; A6; mpkCCD(c14); ENaC; kidney;

D O I：

10.1016/j.ygcen.2005.11.010

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

High-resistance epithelia derived from amphibian sources such as frog skin, toad urinary bladder, and the A6 Xenopus laevis kidney cell line have been widely used to elucidate the underlying mechanisms involved in the regulation of vectorial ion transport. More recently, the isolation of high-resistance mammalian cell lines has provided model systems in which to study differences and similarities between the regulation of ion transporter function in amphibian and mammalian renal epithelia. In the present study, we have compared the natriferic (Na+ retaining) responses to aldosterone, insulin, and vasotocin/vasopressin in the A6 and mpkCCD(cl4) (mouse principal cells of the kidney cortical collecting duct) cell lines. The functional responses of the epithelial Na+ channel (ENaC) to hormonal stimulation were remarkably similar in both the amphibian and mammalian lines. In addition, insulin- and aldosterone-stimulated, reabsorptive Na+ transport in both cell lines requires the presence of functional PI3-kinase. (c) 2005 Elsevier Inc. All rights reserved.

引用

页码：85 / 92

页数：8

共 36 条

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[2] Phosphoinositide 3-kinase is required for aldosterone-regulated sodium reabsorption [J].