Proteomic analysis of isolated mouse distal convoluted tubules following high potassium or low sodium diet
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ABSTRACT: The “aldosterone paradox” is a poorly understood physiological mechanism in which increases in the hormone aldosterone either serve to stabilize blood pressure by increasing sodium-chloride (NaCl) reabsorption or to excrete potassium (K+). Under low NaCl intake, abundance and activity of the thiazide-sensitive NaCl cotransporter NCC, expressed in the distal convoluted tubule (DCT), is high, whereas it is low during high K+ intake - leading to increased delivery of NaCl to downstream segments and increased electrogenic K+ secretion. Despite a critical role in blood pressure and K+ homeostasis, little is known about the molecular alterations in the DCT during the aldosterone paradox, and how they control NCC levels. The objective of this study was to define the proteome of the DCT and how it is modified by increased circulating aldosterone levels subsequent to long-term low dietary NaCl or high K+ intake.
INSTRUMENT(S): Q Exactive
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): Epithelial Cell, Kidney
SUBMITTER: Qi Wu
LAB HEAD: Robert A. Fenton
PROVIDER: PXD014383 | Pride | 2021-03-30
REPOSITORIES: Pride
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