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The mechanisms involved in the release of Metenkephalin-like immunoreactivity (MLI) into the circulation following oral administration of ethanol and chlorpropamide were investigated in dogs. The origin of plasma MLI and the sites where it may be metabolized were also studied. Moreover, the molecular nature of circulating MLI was characterized.

In conscious animals oral administration of ethanol (0·15 ml/kg) led to a significant (P<0·01) rise in plasma MLI concentrations in chlorpropamidepretreated animals from a basal level of 43 ± 6 (mean ± S.E.M.) to a peak of 66 ± 8 ng/l. Similar rises in MLI concentrations were observed following administration of ethanol with disulfiram and ethanol with chlorpropamide and captopril. In contrast, the administration of ethanol alone or ethanol with 4-methylpyrazole resulted in a decrease in plasma MLI concentrations.

Comparisons of two different doses of i.v. acetaldehyde, the first metabolite of ethanol, showed that plasma MLI concentrations rose significantly (P<0·05) only after the larger dose (8 mg/kg), rising from 45±7 to 81 ± 18 ng/l. These results suggest that acetaldehyde is the active component in the chlorpropamide+ ethanol-induced MLI secretion.

Plasma MLI was also measured following acetaldehyde infusion in adrenalectomized dogs with and without hexamethonium treatment. Acute bilateral adrenalectomy resulted in a decrease (P<0·05) in plasma MLI concentrations, but the levels remained detectable. Moreover, subsequent acetaldehyde infusion led to rises in plasma MLI similar to those observed in animals with intact adrenals. These MLI responses were not altered by the concurrent i.v. administration of hexamethonium. Gel filtration chromatography revealed that Met-enkephalin exists in the circulation predominantly in larger molecular forms with approximate sizes of 18 000 and 8000 Da in the basal state, after stimulation and following adrenalectomy.

Journal of Endocrinology (1989) 120, 473–480