Decreased activity of adrenal S-adenosylmethionine decarboxylase in rats subjected to dopamine agonists, metabolic stress, or bodily immobilization.
The activity of S-adenosylmethionine decarboxylase (SAM-DC) has been measured in the adrenal gland of rats given treatments that are known to result in increased activity of ornithine decarboxylase in this organ. In contrast to the effects of the dopamine agonists piribedil and apomorphine on the latter enzyme, the administration of these drugs caused decreases of SAM-DC in both parts of the gland. After piribedil the activity decreased rapidly to a minimum at 2-4 h, with recovery by 6 h. The stress of immobilization or the administration of insulin or 2-deoxyglucose (2-DG) also decreased adrenal SAM-DC activity. The results contrast with those observed in other rat tissues where SAM-DC is generally induced by treatments that induce ornithine decarboxylase. Denervation of the adrenal gland did not clearly affect the reduction in adrenomedullary SAM-DC after 2-DG. Hypophysectomy resulted in reduced SAM-DC activity in both adrenal medulla and cortex; the activity could be restored by giving the animals 2 IU ACTH daily for 4 days. These changes in activity were parallelled by changes in immunoreactive protein. 2-DG did not decrease SAM-DC in hypophysectomized rats receiving maintenance ACTH dosage. This indicates the presence of hormonal control over the activity of SAM-DC in the adrenal medulla and cortex. Acute administration of an additional 10 IU ACTH to hypophysectomized rats on maintenance dosage of ACTH resulted in decreased SAM-DC activity in both adrenal medulla and cortex. These decreases were not abolished by inhibition of corticosteroid synthesis with metopirone. PRL and GH had no significant effect on adrenal SAM-DC activity of hypophysectomized rats. The reduction of SAM-DC activity in both parts of the gland of hypophysectomized rats with administration of (Bu)2cAMP suggests that cAMP may mediate the decreases in SAM-DC caused by the above treatments.
D012437:Adenosylmethionine Decarboxylase / Q000378:metabolism*; D000302:Adrenal Cortex / Q000201:enzymology; D000311:Adrenal Glands / Q000187:drug effects / Q000201:enzymology* / Q000294:innervation; D000313:Adrenal Medulla / Q000201:enzymology; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001971:Bromocriptine / Q000494:pharmacology; D002262:Carboxy-Lyases / Q000378:metabolism*; D000242:Cyclic AMP / Q000502:physiology; D003714:Denervation; D003847:Deoxyglucose / Q000494:pharmacology; D004298:Dopamine / Q000502:physiology*; D007016:Hypophysectomy; D007328:Insulin / Q000494:pharmacology; D008297:Male; D010891:Piribedil / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012149:Restraint, Physical; D013153:Splanchnic Nerves / Q000502:physiology; D013312:Stress, Physiological / Q000201:enzymology*
D007328:Insulin; D001971:Bromocriptine; D000324:Adrenocorticotropic Hormone; D003847:Deoxyglucose; D010891:Piribedil; D000242:Cyclic AMP; D002262:Carboxy-Lyases; D012437:Adenosylmethionine Decarboxylase; D001058:Apomorphine; D004298:Dopamine