Titlebook: Cholecystokinin Antagonists in Gastroenterology; Basic and Clinical S Guido Adler,Christoph Beglinger Book 1991 Springer-Verlag Berlin Heid

Water-Brash

Boc-Tyr(SO3H)-Nle-Gly-Trp-Nle-Asp-2-Phenylethyl Ester — JMV180: A Unique CCK Analogue with DifferentCCK molecule, more particularly the C-terminal phenylalanine residue, was of crucial importance for the complete biological activity of CCK analogues, both in the peripheral system and in the CNS. Suppression of the C-terminal phenylalanine residue, e.g., Z-CCK-27–32-NH. [Z-Tyr(SO.H)-Met-Gly-Trp-Met

痴呆

Cholecystokinin Receptor Antagonists In Vitrogonist, five different classes of CCK receptor antagonists have been described in various in vitro studies (Tables 1, 2) [30,31]. Members of at least two of these classes [i.e., amino acid derivatives such as lorglumide (CR 1409) or loxiglumide (CR 1505) and substituted benzodiazepine analogues such

Ventricle

Effects of Cholecystokinin Receptor Antagonists in Animal Modelsgonists of CCK’s action on exocrine pancreatic secretion of protein and enzymes in vivo. The antagonists display the same rank order of potency in antagonizing CCK’s action on the pancreas in vivo as that which they show in antagonizing CCK’s action and binding in vitro [4–6,17,46] (Fig. 1). However

媒介

Effect of MK-329 on Pancreatic Secretion in Manolecystokinin (CCK) is generally regarded as an important stimulant of the postprandial pancreatic enzyme output based on studies where the enzyme response to physiological doses of exogenous CCK have been compared to the food stimulated response [1,2]. Most of these studies have concluded that post

勉强

Regulation of Gallbladder Contraction and Gastric Emptying by the CCK Receptor Antagonist MK-329er contraction and pancreatic protein secretion as well as regulation of gastric emptying, stimulation of intestinal motility, stimulation of insulin secretion, and induction of satiety [23]. However, it has been difficult to establish whether these are pharmacologic or true physiologic actions of C

FACET

Regulation of CCK Release by Bile Acidscids into the duodenum. Together with monoglycerides and phospholipids, bile acids form mixed micelles to facilitate fat absorption. Eventually, 95% of them are reabsorbed by the terminal ileum to finish the enterohepatic cycle [4]. Since bile acids presumably get in contact with intestinal CCK cell

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