Infusions of tolbutamide (1 mg./kg. min.), glibenclamide (2.5 μg./kg. min.), or glymidine Na (1 mg./kg. min.) in ducks produced a prompt fall in plasma immunoreactive glucagon (IRG), a prompt rise in plasma immunoreactive insulin (IRI) and a subsequent fall in plasma glucose. In dogs, the infusions of these three sulfonamide drugs also caused a rise in IRI and subsequent hypoglycemia, but no specific changes in IRG level in the pancreatic vein and the femoral artery. The infusion of glibenclamide (0.013 μg./kg. min.) into the pancreatic artery of a dog increased IRI secretion and produced a fall in plasma glucose but did not affect IRG level in the pancreatic vein. Carboxytolbutamide, which lacks hypoglycemic activity, failed to influence IRG and IRI in ducks.

The results suggest that the hypoglycemic effect of sulfonamide drugs is mediated by insulin release and, in ducks but not in dogs, by suppression of glucagon secretion. The cause of this species difference is unknown, but the present results and additional data suggest that ducks may be much more dependent than dogs on glucagon for carbohydrate metabolism.

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