Transcriptional and physiological responses to chronic ACTH treatment by the mouse kidney.

Physiological Genomics
Donald R DunbarMatthew A Bailey

Abstract

We investigated the effects on urinary steroid and electrolyte excretion and renal gene expression of chronic infusions of ACTH in the mouse. ACTH caused a sustained increase in corticosteroid excretion; aldosterone excretion was only transiently elevated. There was an increase in the excretion of deoxycorticosterone, a weak mineralocorticoid, to levels of physiological significance. Nevertheless, we observed neither antinatriuresis nor kaliuresis in ACTH-treated mice, and plasma renin activity was not suppressed. We identified no changes in expression of mineralocorticoid target genes. Water turnover was increased in chronic ACTH-treated mice, as were hematocrit and hypertonicity: volume contraction is consistent with high levels of glucocorticoid. ACTH-treated mice exhibited other signs of glucocorticoid excess, such as enhanced weight gain and involution of the thymus. We identified novel ACTH-induced changes in 1) genes involved in vitamin D (Cyp27b1, Cyp24a1, Gc) and calcium (Sgk, Calb1, Trpv5) metabolism associated with calciuria and phosphaturia; 2) genes that would be predicted to desensitize the kidney to glucocorticoid action (Nr3c1, Hsd11b1, Fkbp5); and 3) genes encoding transporters of enzyme systems associated with...Continue Reading

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Citations

Sep 14, 2011·Cardiovascular Drugs and Therapy·Ping LuoChangping Hu
Feb 19, 2014·The Journal of Physiology·Robert W HunterMatthew A Bailey
Feb 11, 2015·Current Opinion in Pharmacology·Robert W Hunter, Matthew A Bailey
Nov 16, 2017·Current Hypertension Reports·Matthew A Bailey
May 25, 2021·Pflügers Archiv : European journal of physiology·Linda MullinsJohn Mullins
Aug 3, 2021·Biochemical and Biophysical Research Communications·Usman M AshrafSivarajan Kumarasamy

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E-MEXP-1761

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ELISAs
ELISA
PCR

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Rank Products ( RankProd )
Limma
Webgestalt
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Bioconductor
GCOS

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