title: Adrenocortical response to tail-suspension in young and old rats.
abstract: We recently showed that increased glucocorticoid secretion aggravates disuse atrophy when induced by skeletal unloading. Disuse atrophy in the elderly is becoming a serious problem in many developed countries. In this study we attempted to examine how aging affects the glucocorticoid response to skeletal unloading. Three groups of rats (aged 5 weeks, 12 months and 18 months) were subjected to 7 days of hind limb unloading by tail-suspension. Urinary excretion of corticosterone over a 24-hr period were monitored every other day. Corticosterone excretion in the control group of 5-week-old rats was initially 87.4 +/- 12.8 ng/day and did not change throughout the experiment. Tail-suspension experiments yielded a significant increase (more than 3 fold) in excretion on days 1 and 3 of the suspension before returning to control levels. In the 12-month-old rats, a marked increase in the basal corticosterone level was observed in the control rats throughout the experiment, while the increase by tail-suspension was attenuated with a transient, significant increase on day 5. In 18-month-old rats, a further increase in the basal level was observed in the control group, although excretions tended to increase steadily from day 1 to day 3 and remained high until day 7. Urinary excretion of corticosterone among the 18-month-old suspension group was similar to those observed in the control group. These results indicate that the younger (5-week-old) rats adapted the stress load caused either by tail-suspension or manipulation alone faster than the older rats did (12 or 18 months old). The observation that basal corticosterone excretion increases with age suggests, alterations in the hypothalamic-pituitary-adrenal axis among the aged rats which might aggravates disuse atrophy induced by skeletal unloading.
authors.affiliation: Department of Endocrinology and Metabolism, Division of Molecular and Cellular Adaptation, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Kawano
authors.forename: S
authors.initials: S
authors.lastname: Ohmori
authors.forename: K
authors.initials: K
authors.lastname: Kanda
authors.forename: T
authors.initials: T
authors.lastname: Ito
authors.forename: Y
authors.initials: Y
authors.lastname: Murata
authors.forename: H
authors.initials: H
authors.lastname: Seo
mesh_terms: D000222:Adaptation, Physiological; D000311:Adrenal Glands / Q000033:anatomy & histology / Q000254:growth & development; D000367:Age Factors; D000375:Aging / Q000502:physiology*; D000818:Animals; D001835:Body Weight; D003345:Corticosterone / Q000378:metabolism* / Q000652:urine; D019417:Hindlimb Suspension; D008297:Male; D009133:Muscular Atrophy / Q000503:physiopathology; D009929:Organ Size; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological / Q000378:metabolism* / Q000652:urine
chemical_list: D003345:Corticosterone