The time-course effect of bilateral adrenalectomy on the monoamine oxidase activity of peripheral tissues of the rat



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The monoamine oxidase (MAO) activity of various peripheral tissues of the rat and serum corticosterone levels (SCI) were assayed at various time periods (8 hours, 1, 5, 10, 20, 30 and 40 days) following bilateral adrenalectomy (AX). Of the organs studied, only the MAO activity of the rat heart and vasa deferentia (VD) showed distinct time-related increases above control, sham-operated values. The increase in the VD preceded that of the heart, but the percentage rise was smaller and the effect less sustained. Thus the MAO activity in the VD was first significantly increased after 1 day, whereas 10 days were required for the heart. However, cardiac MAO activity was still elevated at 30 and 40 days, whereas, no significant increase remained in the VD. Liver MAO was slightly but significantly increased at 30 and 40 days but no changes occured in the MAO activity of the spleen and kidney. Thus AX specifically affects the MAO of certain organs but not others and the time-course of this effect seems characteristic for the particular organ. In addition, a positive correlation between both body weight and heart v/eight was found for control MAO activity; this correlation was absent in AX rats. These findings may lend support to a previous proposal that AX affects only the MAO located within the cardiac adrenergic fibers. There was also a strong correlation between increases in MAO activity and markedly reduced SCL. However, no evidence was obtained for any progressive return in these latter levels with time. Dexamethasone (DEX), administered between 10 and 20 days reversed the rise in cardiac MAO activity. Thus, at least for the heart, a low level of circulating glucocorticoids appears to be totally responsible for the maintenance of the elevated MAO activity. DEX is not an MAO inhibitor, since it failed to alter the cardiac MAO activity in the control rats. Acute experiments (8 hours) were made to compare the effects of metapyrone (an inhibitor of corticosteroid synthesis), epinephrine (E) and AX. All treatments tended to increase MAO activity in the heart, VD and liver, but no such tendency was seen for the kidney. SCI were decreased maximally by AX compared with metapyrone, whereas E increased SCI to approximately 60% above control values. Metapyrone failed to significantly alter the liver MAO activity in vitro. These data failed to confirm previous reports of a rapid increase in the MAO activity of rat organs following metapyrone (4 and 8 hours) and suggests that circulating E might possibly influence MAO by a mechanism unrelated to steroid lack. In conclusion, it is suggested that steroid insufficiency might lead to an increased synthesis rate of MAO at the level of adrenergic cell bodies. The differential time-course effect on the VD and heart may then be related to the known anatomical differences in fiber length which in turn may reflect time differences incurred during axoplasmic transport of the new formed enzyme.