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Glucocorticoids increase salt appetite by increasing urinary excretion
Author(s) -
Thunhorst Robert L.,
Beltz Terry,
Johnson Alan Kim
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a508
Subject(s) - appetite , endocrinology , ingestion , excretion , medicine , chemistry , sodium , glucocorticoid , mineralocorticoid , organic chemistry
Deoxycorticosterone acetate (DOCA) acts in the brain to stimulate salt appetite. Glucocorticoids greatly potentiate salt appetite during DOCA treatment, possibly by augmenting central actions of DOCA. However, glucocorticoids have powerful renal effects to promote excretion of water and sodium that might indirectly affect salt appetite by increasing excretion of the ingested sodium load. We addressed this possibility by determining water and sodium intakes, excretions and balances during daily injections of DOCA, the glucocorticoid agonist dexamethasone (DEX) and their co‐administration (DOCA+DEX). During DOCA, water and sodium intakes exceeded their urinary excretion yielding positive water and sodium balances and weight gain indicative of fluid retention. During DEX, water and sodium excretion outpaced ingestion resulting in negative balances for both and weight loss. During DOCA+DEX, sodium ingestion greatly increased and sodium balance was positive. However, water excretion exceeded fluid ingestion yielding markedly negative water balances and weight loss. We conclude that glucocorticoids may increase salt appetite during DOCA treatment by increasing urinary excretion of water and thereby preventing fluid retention. Supported by NIH grants AG025465 to RLT and HL14388, HL57472 and DK066086 to AKJ.