ArticleProceedings of the National Academy of Sciences of the United States of America1998
Mineralocorticoid receptor knockout mice: pathophysiology of Na+ metabolism.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.
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Who cites it
120 citing papers in PubMed.
- Aldosterone synthase inhibition: cardiorenal protection in animal disease models and translation of hormonal effects to human subjects.Journal of translational medicine · 2014Trial
- Balancing inflammation under stress: glucocorticoid regulation of innate immune pathways.Bioscience reports · 2026Review
- Interplay Between the Mineralocorticoid System, Inflammation, Hypertension, and Kidney Disease.Kidney360 · 2025Review
- Contemporary evidence of non-steroidal mineralocorticoid receptor antagonists in cardio-kidney-metabolic syndrome.Future cardiology · 2025Review
- Impact of aldosterone deficiency on the development of diuretic resistance in mice.Pflugers Archiv : European journal of physiology · 2025Article
- Prenatal exposure to the mineralocorticoid receptor antagonist spironolactone disrupts hippocampal area CA2 connectivity and alters behavior in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Aldosterone-independent regulation of K + secretion in the distal nephron.Current opinion in nephrology and hypertension · 2024Review
- Review
- The Mineralocorticoid Receptor in the Vasculature: Friend or Foe?Annual review of physiology · 2024Review
- Extra-adrenal aldosterone: a mini review focusing on the physiology and pathophysiology of intrarenal aldosterone.Endocrine · 2024Review
- Glucocorticoids, their uses, sexual dimorphisms, and diseases: new concepts, mechanisms, and discoveries.Physiological reviews · 2024Review
- The Mineralocorticoid Receptor Plays a Crucial Role in Macrophage Development and Function.Endocrinology · 2023Article
- Effects of Corticosterone on the Excitability of Glutamatergic and GABAergic Neurons of the Adolescent Mouse Superficial Dorsal Horn.Neuroscience · 2023Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Acute deletion of the central MR/GR steroid receptor correlates with changes in LTP, auditory neural gain, and GC-A cGMP signaling.Frontiers in molecular neuroscience · 2023Article
- Article
- A Case of a Pregnant Woman With Primary Aldosteronism and Superimposed Preeclampsia Treated With Esaxerenone.Journal of the Endocrine Society · 2022Article
- Regulation of distal tubule sodium transport: mechanisms and roles in homeostasis and pathophysiology.Pflugers Archiv : European journal of physiology · 2022Review
- Loss of central mineralocorticoid or glucocorticoid receptors impacts auditory nerve processing in the cochlea.iScience · 2022Article
- Domestication of farmed fishFrontiers in endocrinology · 2022Review
60 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mineralocorticoid receptor (MR)-deficient mice were generated by gene targeting. These animals had a normal prenatal development. During the first week of life, MR-deficient (-/-) mice developed symptoms of pseudohypoaldosteronism. They finally lost weight and eventually died at around day 10 after birth from dehydration by renal sodium and water loss. At day 8, -/- mice showed hyperkalemia, hyponatremia, and a strong increase in renin, angiotensin II, and aldosterone plasma concentrations. Methods were established to measure renal clearance and colonic transepithelial Na+ reabsorption in 8-day-old mice in vivo. The fractional renal Na+ excretion was elevated >8-fold. The glomerular filtration rate in -/- mice was not different from controls. The effect of amiloride on renal Na+ excretion and colonic transepithelial voltage reflects the function of amiloide-sensitive epithelial Na+ channels (ENaC). In -/- mice, it was reduced to 24% in the kidney and to 16% in the colon. There was, however, still significant residual ENaC-mediated Na+ reabsorption in both epithelia. RNase protection analysis of the subunits of ENaC and (Na++ K+)-ATPase did not reveal a decrease in -/- mice. The present data indicate that MR-deficient neonates die because they are not able to compensate renal Na+ loss. Regulation of Na+ reabsorption via MR is not achieved by transcriptional control of ENaC and (Na+ + K+)-ATPase in RNA abundance but by transcriptional control of other as yet unidentified genes. MR knockout mice will be a suitable tool for the search of these genes.
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