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|Title:||Aldosterone increases Na<sup>+</sup>-K<sup>+</sup>-ATPase activity in skeletal muscle of patients with Conn's syndrome|
Department of Research Centre
Faculty of Medicine, Ramathibodi Hospital, Mahidol University
|Citation:||Clinical Endocrinology. Vol.74, No.2 (2011), 152-159|
|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. © 2011 Blackwell Publishing Ltd.|
|Appears in Collections:||Scopus 2011-2015|
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