CCK-A receptors mediate the effect of cholecystokinin on vasopressin but not on cortisol in pigs.

Abstract

Bolus intravenous injections of cholecystokinin (CCK) octapeptide induce a rapid rise in plasma vasopressin and a later increase in cortisol in the prepubertal pig. To determine whether these endocrine responses involve CCK-A or CCK-B receptors, this experiment investigated the effect of CCK (1 microgram/kg) in pigs (n = 7) pretreated with the CCK-A antagonist L 364718 (70 microgram/kg) or the CCK-B antagonist L 365260 (10 ng/kg and 10 micrograms/kg). The animals were prepared with jugular vein catheters and given the antagonist vehicle, L 364718, or L 365260 10 min before administration of CCK or saline. Analysis of hormone concentrations in blood samples taken 2, 5, 10, and 20 min after the second injection indicated that an abrupt rise in vasopressin, detectable within 2 min of CCK administration, occurred after vehicle or L 365260 pretreatment but not when CCK was preceded by L 364718. In contrast, the rise in plasma cortisol that was observed approximately 15 min after CCK injection was not prevented by either antagonist. Thus peripherally administered CCK induces vasopressin release by CCK-A receptor activation, in agreement with its inhibitory effect on food intake in this species. However, the effect of CCK on cortisol secretion does not appear to involve either CCK-A or CCK-B receptors.