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miR-324-5p and miR-30c-2-3p Alter Renal Mineralocorticoid Receptor Signaling under Hypertonicity.
Cells
April 2022
Physiologie et Physiopathologie Endocriniennes, Université Paris-Saclay, Inserm, 94276 Le Kremlin-Bicêtre, France.
The Mineralocorticoid Receptor (MR) mediates the sodium-retaining action of aldosterone in the distal nephron, but mechanisms regulating MR expression are still poorly understood. We previously showed that RNA Binding Proteins (RBPs) regulate MR expression at the post-transcriptional level in response to variations of extracellular tonicity. Herein, we highlight a novel regulatory mechanism involving the recruitment of microRNAs (miRNAs) under hypertonicity.
View Article and Find Full Text PDFmTORC1 Deficiency Modifies Volume Homeostatic Responses to Dietary Sodium in a Sex-Specific Manner.
Endocrinology
May 2020
Division of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital, Boston, MA.
The mechanistic target of the rapamycin (mTOR) pathway plays a role in features common to both excess salt/aldosterone and cardiovascular/renal diseases. Dietary sodium can upregulate mTORC1 signaling in cardiac and renal tissue, and the inhibition of mTOR can prevent aldosterone-associated, salt-induced hypertension. The impact of sex and age on mTOR's role in volume homeostasis and the regulation of aldosterone secretion is largely unknown.
View Article and Find Full Text PDFRNA-binding protein HuR enhances mineralocorticoid signaling in renal KC3AC1 cells under hypotonicity.
Cell Mol Life Sci
December 2017
Inserm U1185, Faculté de Médecine Paris-Sud, Université Paris-Saclay, 63 rue Gabriel Peri, 94276, Le Kremlin-Bicêtre, France.
Mineralocorticoid receptor (MR) mediates the sodium-retaining action of aldosterone in the distal nephron. Herein, we decipher mechanisms by which hypotonicity increases MR expression in renal principal cells. We identify HuR (human antigen R), an mRNA-stabilizing protein, as an important posttranscriptional regulator of MR expression.
View Article and Find Full Text PDFAfter the discovery of aldosterone (1953), many synthetic steroids were tested for their ability to block the sodium retaining and potassium excreting effect of synthetic mineralocorticoids in adrenalectomized rats. In the same years Kagawa discovered that 17-spirolactone steroids were effective to block mineralocorticoid effects, but when used alone they did not produce any effect in adrenalectomized rats. After the description of the first case of primary aldosteronism (1955), spironolactone (SP) was considered the main treatment before surgery to control blood pressure and kaliemia and for long-term treatment in patients with bilateral adrenal hyperplasia.
View Article and Find Full Text PDFUrinary excretion of AQP2 and ENaC in autosomal dominant polycystic kidney disease during basal conditions and after a hypertonic saline infusion.
Am J Physiol Renal Physiol
April 2012
Dept. of Medical Research, Holstebro Hospital, Lægaardvej 12, Holstebro, Denmark.
Renal handling of sodium and water is abnormal in chronic kidney diseases. To study the function and regulation of the aquaporin-2 water channel (AQP2) and the epithelial sodium channel (ENaC) in autosomal dominant polycystic kidney disease (ADPKD), we measured urinary excretion of AQP2 (u-AQP2), the β-subunit of ENaC (u-ENaC(β)), cAMP (u-cAMP), and prostaglandin E(2) (u-PGE(2)); free water clearance (C(H2O)); fractional sodium excretion (FE(Na)); and plasma vasopressin (p-AVP), renin (p-Renin), angiotensin II (p-ANG II), aldosterone (p-Aldo), and atrial and brain natriuretic peptide (p-ANP, p-BNP) in patients with ADPKD and healthy controls during 24-h urine collection and after hypertonic saline infusion during high sodium intake (HS; 300 mmol sodium/day) and low sodium intake (LS; 30 mmol sodium/day). No difference in u-AQP2, u-ENaC(β), u-cAMP, u-PGE(2), C(H2O), and vasoactive hormones was found between patients and controls at baseline, but during HS the patients had higher FE(Na).
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