Peer-reviewed veterinary case report
Muscle enzyme changes in dogs with pituitary-dependent Cushing's
By Schotanus, B A et al.·Published in Domestic animal endocrinology·2006·Department of Pathobiology, Netherlands·View original on PubMed →
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Original publication title: Na(+), K(+)-ATPase content in skeletal muscle of dogs with pituitary-dependent hyperadrenocorticism.
- Species:
- dog
Plain-English summary
A group of dogs with pituitary-dependent hyperadrenocorticism (PDH), a condition that causes excessive hormone production, showed muscle weakness and reduced endurance due to lower levels of a key enzyme (Na(+), K(+)-ATPase) in their muscle cells. After undergoing surgery to remove the pituitary gland and receiving hormone replacement therapy, these dogs had improved enzyme levels, which helped restore their muscle function. This suggests that treating PDH can help improve muscle strength and endurance in affected dogs.
People also search for: dog muscle weakness treatment · pituitary-dependent hyperadrenocorticism in dogs · dog endurance problems · hormone replacement for dogs with PDH
Abstract
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.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/16202554/