Na(+), K(+)-ATPase content in skeletal muscle of dogs with pituitary-dependent hyperadrenocorticism.
Several hormones regulate Na(+), K(+)-ATPase content in the muscle cell membrane, which is essential for maintaining muscle cell excitability. Chronic glucocorticoid excess is associated with muscle weakness and reduced endurance. We hypothesized that chronic glucocorticoid excess affects Na(+), K(+)-ATPase content in canine skeletal muscle, and contributes to reduced endurance and muscle weakness associated with pituitary-dependent hyperadrenocorticism (PDH) in dogs. Therefore, Na(+), K(+)-ATPase content in skeletal muscle was evaluated before and after hypophysectomy and hormone replacement (cortisone and l-thyroxin) in dogs with PDH (n=13), and in healthy controls (n=6). In addition, baseline and exercise-induced changes in plasma electrolyte concentrations and acid-base balance were evaluated before and after hypophysectomy in dogs with PDH. Na(+), K(+)-ATPase content of gluteal muscle in dogs with PDH was significantly lower than in control dogs (201+/-13pmol/g versus 260+/-8pmol/g wet weight; P<0.01). Similar differences were found in palatine muscle. After hypophysectomy and on hormone replacement, Na(+), K(+)-ATPase was increased (234+/-7pmol/g wet weight). Both plasma pH and base excess in dogs with PDH (7.44+/-0.01; 1.7+/-0.6mmol/l, respectively) were significantly higher (P<0.05) than after hypophysectomy and hormone replacement (7.41+/-0.01; -0.2+/-0.4mmol/l, respectively). Exercise induced respiratory alkalosis, but did not result in hyperkalemia in dogs with PDH. In conclusion, chronic glucocorticoid excess in dogs with PDH is associated with decreased Na(+), K(+)-ATPase content in skeletal muscle. This may contribute to reduce endurance in canine PDH, although dogs with PDH did not exhibit exercise-induced hyperkalemia. Na(+), K(+)-ATPase content normalized to values statistically not different from healthy controls after hypophysectomy and hormone replacement.
Schotanus
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Department of Pathobiology, Division of Anatomy and Physiology, Faculty of Veterinary Medicine, Utrecht University, PO Box 80.158, 3508 TD Utrecht, The Netherlands.
Meij
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BP
Vos
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Kooistra
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Everts
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ME
D000308:Adrenocortical Hyperfunction / Q000201:enzymology / Q000209:etiology / Q000662:veterinary*; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D001769:Blood; D004283:Dog Diseases / Q000201:enzymology*; D004285:Dogs; D005260:Female; D005938:Glucocorticoids / Q000097:blood; D013006:Growth Hormone / Q000097:blood; D020249:Hormone Replacement Therapy / Q000662:veterinary; D006854:Hydrocortisone / Q000097:blood; D006863:Hydrogen-Ion Concentration; D007016:Hypophysectomy / Q000662:veterinary; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008297:Male; D018482:Muscle, Skeletal / Q000201:enzymology*; D010042:Ouabain / Q000378:metabolism; D010807:Physical Endurance; D005082:Physical Exertion; D010911:Pituitary Neoplasms / Q000150:complications / Q000601:surgery / Q000662:veterinary*; D000254:Sodium-Potassium-Exchanging ATPase / Q000032:analysis*; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014316:Tritium
D005938:Glucocorticoids; D014316:Tritium; D010042:Ouabain; D007334:Insulin-Like Growth Factor I; D000324:Adrenocorticotropic Hormone; D013972:Thyrotropin; D013006:Growth Hormone; D000254:Sodium-Potassium-Exchanging ATPase; D013974:Thyroxine; D006854:Hydrocortisone