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The aim of this study was to examine the influence of cholecystokinin (CCK)-octapeptide (OP) and its amphibian analogue cerulein infusions on duodenal myoelectric and motor activities, as well as to compare the effects of CCK peptides on duodenal bulb and duodenal motility in non-fasted conscious rams. Five rams underwent implantation of bipolar platinum electrodes to the duodenal bulb, and distal duodenum, as well as a strain gauge force transducer near the duodenal electrode. During continuous myoelectrical and motor recordings, 0.15 M NaCl or CCK peptides were administered intravenously. Infusions of CCK-OP at doses of 5 and 50 ng/kg/min and infusions of cerulein at doses of 0.5 and 1.5 ng/kg/min were applied for 60 min and started 15 min after the onset of the duodenal phase 2b of the migrating motor complex. The higher infusion dose of the CCK-OP in the duodenal bulb triggered the strong inhibitory response within few minutes following the start of infusion while in the duodenum its inhibitory effect was shorter and arrived within 40-50 min following the onset of the infusion. The higher dose of cerulein evoked a reaction similar to CCK-OP response in the duodenal bulb while in the duodenum the clear inhibitory response arrived about 20 min earlier than after CCK-OP. A lower infusion dose of CCK peptides evoked less pronounced effects. It is concluded that CCK-OP inhibits ovine duodenal motility in a dose-and region-specific manner. This effect seems to be physiological.
The effect of CCK-8 (50 ng, i. c. v.) on the neurohypophysial vasopressin and oxytocin storage was estimated in haemorrhaged (1 ml per 100 g b. w.) male Wistar rats. In another experimental series rats dehydrated for three days were given CCK-8 in a daily i. c. v. dose of 50 ng. The neurohypophysial vasopressin and oxytocin content was bioassayed by pressor effect following Dekański or milk- ejection activity in vitro following van Dongen and Hays, respectively. The decrease of neurohypophysial vasopressin and oxytocin content, brought about by dehydration, was significantly less marked in animals treated with CCK-8. The depletion of neurohypophysial vasopressin and oxytocin content in haemorrhaged animals could be completely inhibited by earlier i. c. v. administration of CCK-8. It is suggested that hypothalamic cholecystokinin may serve as a modulator of neurohypophysial function.
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