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We had previously shown that the hypothalamo-neurohypophyseal vasopressin secreting system is suppressed in aged rats. In the present study, using aged (26 months) male Fischer 344 (F344) rats, we showed that in contrast to vasopressin, oxytocin plasma concentration and hypothalamic content were unaltered in comparison with young (2-3 months) rats; however, based on data from our past and current studies, the neurohypophyseal concentrations of both hormones were found to be decreased in aged rats. We also compared the effect of aging on the oxytocin and vasopressin in secretory functions. Superfusion technique was employed to examine oxytocin and vasopressin release from isolated neural lobes of young (2-3 months) and old (26 months) male F344 and young (2-3 months), middle-aged (12 months) and old (30 months) Sprague-Dawley (SD) rats. Aging affected basal release of oxytocin and vasopressin in a differential manner. Expressed per gland, basal release of oxytocin increased in aged rats of both strains; whereas vasopressin release decreased in SD, and did not change in F344, old rats. The vasopressin responses to electrical stimulation, 56 mM K+ and initial traumatic release were decreased in aged rats; whereas oxytocin responses were either unaltered or decreased much less. All age-related changes were more pronounced in SD than in F344 rats. Thus, while the aging process is associated with a significant impairment in the vasopressin secretory function, the oxytocin secretory function is much less affected by that process. Significant strain differences were observed in the effects of aging on oxytocin and vasopressin release.

We studied the effect of aging on vasopressin (VP) release from isolated neurohypophyses (NH) individually superfused with synthetic medium TC 199 with Hanks' salts. The superfusion technique is described in detail. Male Fisher 344 rats 2 months (young, n = 17), 12 months (adult, n = 14) and 30 months (old, n = 17) of age were used. VP was measured by radioimmunoassay (RIA). The age-related VP release was analyzed as follows: initial traumatic release, basal release, VP release evoked by electrical stimulation (10-second trains every 20 s of matched biphasic stimuli, 0.2 ms width, 8 mA, 30 Hz), by chemical stimulation (56 mM K+) and total release for the entire superfusion period. When VP release was expressed per milligram NH, it was significantly lower under all conditions in the old rats than in the young ones. In the adult rats, traumatic, basal and total release values were similar to those of the young rats, whereas their responses to chemical and electrical stimulation were similar to those of old rats. Residual VP content expressed per whole NH was significantly higher in the old and adult rats, reflecting a larger glandular size, but when expressed per milligram NH tissue, it was low in the old rats. The percent of VP released during the entire superfusion period relative to the residual VP content was significantly lower in the old than in the young and adult rats. The magnitude of the maximal VP release exceeding the basal release, in response to electrical and chemical stimulation, was similar in young and old rats. However, in the adult rats it was significantly lower than in both the young and old following chemical stimulation. A significantly larger number of old and adult NHs exhibited a more delayed response to chemical, but not to electrical stimulation, than did the young NHs. These data demonstrate an age-related decrease in VP release in Fisher 344 rats. Since the traumatic and basal VP release in the adult rats is similar to the release in the young rats, while the stimulated release in the adult rats resembles the response of the old animals, the results suggest that an impairment of stimulated VP release occurs at an earlier stage of the aging process than does an impairment of spontaneous (traumatic and basal) release.