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Aldosterone increases Na + ‐K + ‐ATPase activity in skeletal muscle of patients with Conn’s syndrome
Author(s) -
Phakdeekitcharoen Bunyong,
Kittikanokrat Wassana,
Kijkunasathian Chusak,
Chatsudthipong Varanuj
Publication year - 2011
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.2010.03912.x
Subject(s) - medicine , endocrinology , aldosterone , skeletal muscle , hyperaldosteronism
Summary 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 vs 1·02 ± 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.