The secretory effect of sulfated and nonsulfated cholecystokinin octapeptide (CCK-8) was studied on the isolated perfused porcine pancreas. Both CCKs in concentrations from 10^–11 to 10^–8 mol/l in the presence of glucose (7.5, 5.0 or 3.5 mmol/l) were without effect on insulin and glucagon release. The exocrine secretion was stimulated by both CCKs in a dose-dependent manner, but sulfated CCK-8 was considerabley more potent. The study shows that CCK-8, a major constituent of endogenous CCK, does not contribute to the incretin mechanism, irrespective of degree of sulfation. In contrast, CCK-8 is a potent stimulator of exocrine pancreatic secretion. For this effect sulfation is crucial.

Glucose, insulin and glucagon concentrations were determined before, during and after a 60-min period of haemorrhagic hypotension at 60 mm Hg in controls, adrenal-ectomized and splanchnicectomized cats. Peak increase of arterial plasma glucose concentration in response to haemorrhage was 13.7 ± 4.3 mM in controls, 10.2 ± 2.8 mΛf in adrenal-ectomized and 3.1 ± 1.7 mM in splanchnicectomized cats, respectively. Peak portal insulin decrease was 58 ± 8 and 36 ± 14 pmol/l in controls and adrenalectomized cats, respectively, whereas insulin levels increased slightly in splanchnicectomized cats during hypovolaemia. Portal plasma glucagon concentration rose by about 250 pmol/l in response to bleeding in all groups of cats. We conclude that the prompt hyperglycaemic and hypomsuünaemic response to haemorrhage in cats are caused by an adrenergic, ‘non-medullary’ mechanism, whereas the marked rise in pancreatic glucagon release seems due to factors unrelated to the sympatho-adrenal system.

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