Structure-function relationships of peptide fragments of gastrin and cholecystokinin.

1977 ◽  
Vol 233 (4) ◽  
pp. E286
Author(s):  
D L Kaminski ◽  
M J Ruwart ◽  
M Jellinek
Keyword(s):  
Amino Acids ◽  
Structure Function ◽  
Bile Flow ◽  
Hydrogen Ion ◽  
Biliary System ◽  
Peptide Fragments ◽  
Hepatic Bile ◽  
Amino Acid Peptide ◽  
The Common ◽  
Active Fragments

This study evaluates the structure-function relationships of the C-terminal peptide fragments of gastrin and cholecystokinin (CCK) in the biliary system and the stomach. Dogs with chronic biliary and gastric fistulas were used. Administration of the common fragments of CCK and gastrin with four and five amino acids and the active fragments of CCK with six through eight amino acids without sulfation of tyrosine in position 7 failed to alter hepatic bile flow from control values while significantly stimulating gastric hydrogen ion output. Administration of the seven and eight amino acid peptide fragments of CCK with sulfation of tyrosine in position 7 significantly increased hepatic bile flow. Administration of the sulfated octapeptide with 4 microgram/kg per h of nonsulfated octapeptide did not result in the inhibition of the choleresis produced by the sulfated peptide. The gastric hydrogen ion response produced by the administration of the nonsulfated and sulfated peptide was equal to that of the nonsulfated peptide alone. These results suggest that in the biliary system the receptor is highly specific as sulfation of the peptide fragment of CCK is essential for combining with the receptor, whereas in the stomach the receptor has little specificity and combines with all of the peptide fragments evaluated.

Fasting and postprandial hepatic bile flow in unanesthetized opossums

1990 ◽  
Vol 259 (5) ◽  
pp. G745-G752 ◽  
Author(s):  
I. Takahashi ◽  
M. K. Kern ◽  
W. J. Dodds ◽  
W. J. Hogan ◽  
R. D. Layman ◽  
...  
Keyword(s):  
Bile Acid ◽  
Bile Flow ◽  
Common Duct ◽  
Enterohepatic Circulation ◽  
Phase Iii ◽  
Hepatic Bile ◽  
Bipolar Electrodes ◽  
Motor Complex ◽  
The Common ◽  
The Relationship

In conscious opossums, we evaluated the relationship between hepatic bile flow and the intestinal motor function during fasting as well as after feeding. In six opossums, bipolar electrodes were implanted from the gastric antrum to the terminal ileum. After cholecystectomy, the common duct was ligated, and a catheter was tied into the proximal common duct for collecting hepatic bile. During subsequent studies, hepatic bile flow was measured, and bile was returned to the duodenum through an externalized duodenal catheter. Cyclic increases in bile flow during fasting did not show a close correlate with the duodenal migratory motor complex (MMC) cycle. Rather, bile flow showed peak values [0.11 +/- 0.02 (SE) ml/min] when phase III MMC activity reached the midileum. Hepatic bile flow correlated closely with the amount of bile acid secreted by the liver. When the bile acid pool was depleted by diverting bile from the intestine, hepatic secretion of bile fell to uniformly low values of approximately 0.04 ml/min that did not show cyclic variation. Hepatic bile flow after feeding increased to a maximal value of 0.12 +/- 0.01 ml/min at 90 min. We conclude that increases in hepatic bile flow during fasting and after meals are determined mainly by variations in intestinal motor activity that alter small bowel transit and thereby affect the enterohepatic circulation of bile acids.

Effect of the histamine (H2) inhibitor metiamide on histamine-stimulated bile flow in dogs

1976 ◽  
Vol 231 (2) ◽  
pp. 516-521 ◽  
Author(s):  
DL Kaminski ◽  
MJ Ruwart ◽  
M Jellinek
Keyword(s):  
Bile Flow ◽  
Competitive Inhibition ◽  
Acid Output ◽  
Hydrogen Ion ◽  
Receptor Interaction ◽  
Maximal Response ◽  
H2 Receptor Antagonist ◽  
Hepatic Bile ◽  
Histamine H2 Receptor ◽  
H2 Receptor

The effects of the histamine H2-receptor inhibitor metiamide on histamine-stimulated canine bile flow and gastric hydrogen ion output were evaluated. Histamine was found to stimulate bile volume in doses comparable to those that stimulated gastric hydrogen ion output; both responses appeared to have the same maximal response dose, 150 mug/kg per h. Metiamide alone did not alter hepatic bile flow. Administration of metiamide, 2 mg/kg per h, along with various doses of histamine demonstrated that the H2-receptor antagonist decreased bile volume and gastric hydrogen ion output from values obtained with histamine administration alone. The D50 of histamine for bile flow was 16.3 mug/kg per h and the D50 for hydrogen ion output was 44.2 mug/kg per h, Kinetic analysis suggests that the decrease in histamine-stimulated hydrogen ion output produced by metiamide is the result of competitive inhibition; the decrease in histamine-stimulated bile volume by metiamide which is different from the hydrogen ion inhibition, suggests noncompetitive inhibition. These data indicate that the mechanism of histamine choleresis is different from the mechanism of histamine-stimulated gastric acid output and that histamine-stimulated bile flow may not be the result of direct hormone-receptor interaction.

History of hepatic bile formation: old problems, new approaches

2014 ◽  
Vol 38 (4) ◽  
pp. 279-285 ◽  
Author(s):  
Norman B. Javitt
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Water Flow ◽  
Bile Flow ◽  
Water Movement ◽  
Sodium Taurocholate ◽  
Biliary System ◽  
Hepatic Bile ◽  
Bile Formation ◽  
Osmotic Effect

Studies of hepatic bile formation reported in 1958 established that it was an osmotically generated water flow. Intravenous infusion of sodium taurocholate established a high correlation between hepatic bile flow and bile acid excretion. Secretin, a hormone that stimulates bicarbonate secretion, was also found to increase hepatic bile flow. The sources of the water entering the biliary system with these two stimuli were differentiated by the use of mannitol. An increase in its excretion parallels the increase in bile flow in response to bile acids but not secretin, which led to a quantitative distinction between canalicular and ductular water flow. The finding of aquaglyceroporin-9 in the basolateral surface of the hepatocyte accounted for the rapid entry of mannitol into hepatocytes and its exclusion from water movement in the ductules where aquaporin-1 is present. Electron microscopy demonstrated that bile acids generate the formation of vesicles that contain lecithin and cholesterol after their receptor-mediated canalicular transport. Biophysical studies established that the osmotic effect of bile acids varies with their concentration and also with the proportion of mono-, di-, and trihydroxy bile acids and provides a basis for understanding their physiological effects. Because of the varying osmotic effect of bile acids, it is difficult to quantify bile acid independent flow generated by other solutes, such as glutathione, which enters the biliary system. Monohydroxy bile acids, by markedly increasing aggregation number, severely reduce water flow. Developing biomarkers for the noninvasive assessment of normal hepatic bile flow remains an elusive goal that merits further study.

scholarly journals Amino Acids and Peptides. LIV. Application of 2-Adamantyl Derivatives as Protecting Groups to the Synthesis of Peptide Fragments Related to Sulfolobus solifataricus Ribnuclease. I.

1999 ◽  
Vol 47 (8) ◽  
pp. 1089-1096 ◽  
Author(s):  
Yoshio OKADA ◽  
Shima JOSHI ◽  
Noriyuki SHINTOMI ◽  
Yukihiro KONDO ◽  
Yuko TSUDA ◽  
...  
Keyword(s):  
Amino Acids ◽  
Protecting Groups ◽  
Peptide Fragments

scholarly journals Urotensin receptor (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

2019 ◽  
Vol 2019 (4) ◽  
Author(s):  
Anthony P. Davenport ◽  
Stephen A. Douglas ◽  
Alain Fournier ◽  
Adel Giaid ◽  
Henry Krum ◽  
...  
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Neurosecretory System ◽  
Urotensin Ii ◽  
High Sequence Identity ◽  
Caudal Neurosecretory System ◽  
Amino Acid Peptide ◽  
Related Peptide ◽  
Human Sequence ◽  
Mature Mouse

The urotensin-II (U-II) receptor (UT, nomenclature as agreed by the NC-IUPHAR Subcommittee on the Urotensin receptor [26, 36, 89]) is activated by the endogenous dodecapeptide urotensin-II, originally isolated from the urophysis, the endocrine organ of the caudal neurosecretory system of teleost fish [7, 88]. Several structural forms of U-II exist in fish and amphibians. The goby orthologue was used to identify U-II as the cognate ligand for the predicted receptor encoded by the rat gene gpr14 [20, 62, 68, 70]. Human urotensin-II, an 11-amino-acid peptide [20], retains the cyclohexapeptide sequence of goby U-II that is thought to be important in ligand binding [53, 11]. This sequence is also conserved in the deduced amino-acid sequence of rat urotensin-II (14 amino-acids) and mouse urotensin-II (14 amino-acids), although the N-terminal is more divergent from the human sequence [19]. A second endogenous ligand for the UT has been discovered in rat [83]. This is the urotensin II-related peptide, an octapeptide that is derived from a different gene, but shares the C-terminal sequence (CFWKYCV) common to U-II from other species. Identical sequences to rat urotensin II-related peptide are predicted for the mature mouse and human peptides [32]. UT exhibits relatively high sequence identity with somatostatin, opioid and galanin receptors [89].

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