Cited by 17Hormonal Regulation and HypertensionPotassium and Related DisordersIon Transport and Channel Regulation

Aldosterone increases Na+-K+-ATPase activity in skeletal muscle of patients with Conn’s syndrome: Aldosterone and skeletal muscle Na+- K+- ATPase

Phakdeekitcharoen, Bunyong, Kittikanokrat, Wassana, Kijkunasathian, Chusak, Chatsudthipong, Varanuj·2011·Clinical Endocrinology

Abstract

OBJECTIVE: In Conn's syndrome, hypokalaemia normally results from renal potassium loss because of the effect of excess aldosterone on Na(+) -K(+) -ATPase in principal cells. Little is known about the effect of aldosterone on cellular potassium redistribution in skeletal muscle. Our study determined the effect of aldosterone on muscle Na(+) -K(+) -ATPase. DESIGN: Muscle biopsies were taken from six patients immediately before and 1 month after adrenalectomy. Ten age-matched subjects with normal levels of circulating aldosterone served as controls. RESULTS: Average plasma aldosterone was significantly higher in presurgery (235·0 ± 51·1 pg/ml) than postsurgery (64·5 ± 25·1 pg/ml) patients. Similarly, Na(+) -K(+) -ATPase activity, relative mRNA expression of α(2) (not α(1) or α(3) ) and β(1) (not β(2) or β(3) ), and protein abundance of α(2) and β(1) subunits were greater in pre- than postsurgery samples (128·7 ± 12·3 vs 79·4 ± 13·3 nmol·mg/protein/h, 2·45 ± 0·31 vs 1·04 ± 0·17, 1·92 ± 0·22 vs1·02 ± 0·14, 2·17 ± 0·33 vs 0·98 ± 0·09 and 1·70 ± 0·17 vs 0·90 ± 0·17, respectively, all P<0·05). The activity and mRNA expression of the α(2) and β(1) subunits correlated well with plasma aldosterone levels (r = 0·71, r = 0·75 and r = 0·78, respectively, all P < 0·01). CONCLUSIONS: Our study provides the first evidence in human skeletal muscle that increased plasma aldosterone leads to increased Na(+) -K(+) -ATPase activity via increases in α(2) and β(1) subunit mRNAs and their protein expressions. The increased activity may contribute in part to the induction of hypokalaemia in patients with Conn's syndrome.

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Crossref · 10.1111/j.1365-2265.2010.03912.x

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Authors
Phakdeekitcharoen, B., Kittikanokrat, W., Kijkunasathian, C., & Chatsudthipong, V.
Affiliations
  • Ramathibodi Hospital (TH)
  • Mahidol University (TH)
Corresponding author
Phakdeekitcharoen, Bunyong
Venue
Clinical Endocrinology
Publisher
Wiley
Published
2011-01-06
Volume
74
Issue
2
Pages
152-159
ISSN
0300-0664 (ISSN-L)
OpenAlex
W2122152516
Cited by
17
References
34
Citations by year
2026: 1 · 2024: 2 · 2022: 2 · 2020: 3 · 2019: 1 · 2016: 3 · 2015: 1 · 2014: 1 · 2013: 3
FWCI
0.72
Type
journal article
Language
en
Open access
closed
Locations
  • Clinical Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Potassium and Related Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
primary aldosteronism, aldosterone, Na+/K+-ATPase, skeletal muscle, hypokalemia, adrenalectomy, Na,K-ATPase beta1 subunit, gene expression, plasma aldosterone, potassium redistribution
MeSH terms
Sodium-Potassium-Exchanging ATPase, Adult, Aldosterone, Female, Humans, Hyperaldosteronism, Male, Middle Aged, Sodium, Dietary, Potassium, Dietary, Muscle, Skeletal, Reverse Transcriptase Polymerase Chain Reaction

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