Effect of a New CCK-Receptor Antagonist, CR 1409, on Pancreatic Growth Induced by Caerulein, CCK-8, Bombesin and Gastrin-Releasing Peptide in the Rat

Digestion ◽  
1989 ◽  
Vol 43 (1-2) ◽  
pp. 66-72 ◽  
Author(s):  
Amor Hajri ◽  
Marc Aprahamian ◽  
Christiane Damgé
Keyword(s):  
Receptor Antagonist ◽  
Gastrin Releasing Peptide ◽  
Pancreatic Growth ◽  
Cck Receptor Antagonist

Reduced cholecystokinin mediates the inhibition of pancreatic growth induced by bile salts

1990 ◽  
Vol 259 (1) ◽  
pp. G86-G92 ◽  
Author(s):  
G. Gomez ◽  
C. M. Townsend ◽  
D. W. Green ◽  
S. Rajaraman ◽  
G. H. Greeley ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Plasma Levels ◽  
Bile Salts ◽  
Sodium Taurocholate ◽  
Physiological Role ◽  
Simultaneous Administration ◽  
Inhibitory Effects ◽  
Pancreatic Growth ◽  
Cck Receptor Antagonist

The effects of luminal bile salts on plasma levels of cholecystokinin (CCK) and growth of the pancreas in mice were studied. Nonfasting levels of plasma CCK in control mice were 8.1 +/- 1.5 pM. Feeding mice a 0.5% (wt/wt) sodium taurocholate-supplemented diet for 1 wk significantly lowered nonfasting levels of plasma CCK to 4.1 +/- 0.5 pM and decreased the total contents of pancreatic DNA by 22%, RNA by 25%, and protein by 24%. All of the inhibitory effects of taurocholate on pancreatic growth were completely reversed by the simultaneous administration of CCK-8 (3 micrograms/kg, 3 times daily). In contrast, intraluminal neutralization of endogenous bile salts by feeding a 4% (wt/wt) cholestyramine-supplemented diet for 1 wk significantly elevated nonfasting levels of plasma CCK to 14.7 +/- 1.5 pM and increased the total contents of pancreatic DNA by 34%, RNA by 40%, and protein by 35%. All of the stimulatory actions of cholestyramine on pancreatic growth were completely abolished by the administration of the highly potent and specific CCK-receptor antagonist L364,718 (1 mg/kg, twice daily). These findings, therefore, indicate that bile salts appear to play a physiological role in pancreatic growth by regulation of plasma levels of CCK.

Effects of the CCK receptor antagonist L364,718 on pancreatic growth in adult and developing animals

1989 ◽  
Vol 257 (4) ◽  
pp. G511-G516 ◽  
Author(s):  
K. A. Zucker ◽  
T. E. Adrian ◽  
A. J. Bilchik ◽  
I. M. Modlin
Keyword(s):  
Receptor Antagonist ◽  
Guinea Pigs ◽  
Normal Growth ◽  
Dietary Manipulation ◽  
Pancreatic Development ◽  
Osmotic Pumps ◽  
Pancreatic Growth ◽  
Old Rats ◽  
Cck Receptor Antagonist

Although exogenous administration of cholecystokinin (CCK) or dietary manipulation to increase circulating CCK have previously been shown to promote pancreatic growth, the role of CCK in controlling normal pancreatic development remains unclear. A potent CCK receptor antagonist, L364,718, was administered to rats, guinea pigs, and hamsters to block the effect of endogenous CCK. Animals were given continuous infusions of L364,718 (25 nmol.kg-1.h-1), CCK octapeptide [(CCK-8) 200 pmol.kg-1.h-1], or both CCK-8 and L364,718 for 14 and 28 days. Adult (4-mo-old) and young (4-wk-old) animals were used. CCK-8 and L364,718 were administered via separate, subcutaneously implanted mini-osmotic pumps. Infusions of CCK-8 alone for 28 days resulted in a 21.7% increase in wet pancreatic weight in 4-wk-old rats and a 22.7% increase in 4-wk-old guinea pigs (both P less than 0.001 compared with controls). Similar increases were found in DNA, RNA, and total protein contents. Coadministration of L364,718 totally blocked the trophic effects of exogenously infused CCK-8 in rats and guinea pigs. Administration of L364,718 alone in hamsters, guinea pigs, and rats for 14 and 28 days failed to alter the normal growth of the pancreas gland as measured by these parameters. Although elevated levels of CCK appear to promote a potent trophic response in the growing pancreas, this regulatory peptide does not appear to be an essential trophic factor for the normal growth of the exocrine pancreas in these animals.

Role of cholecystokinin in induction and maintenance of dietary protein-stimulated pancreatic growth

1992 ◽  
Vol 262 (4) ◽  
pp. G740-G746 ◽  
Author(s):  
G. M. Green ◽  
G. Jurkowska ◽  
F. L. Berube ◽  
N. Rivard ◽  
D. Guan ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Dna Content ◽  
Dietary Protein ◽  
High Protein Diet ◽  
Casein Diet ◽  
Pancreatic Growth ◽  
Weight Protein ◽  
Wet Weight ◽  
Cck Receptor Antagonist

The role of cholecystokinin (CCK) in induction and maintenance of pancreatic growth stimulated by a high-protein diet was investigated. Rats adapted to 5% casein diet were switched to 70% casein for 21 days. MK-329, a CCK receptor antagonist, was administered at 2.5 mg.kg-1.day-1 ip, beginning on day zero (day zero treatment) or day 7 (midcourse treatment) of feeding 70% casein and thereafter. Another group was returned to 5% casein after 7 days of feeding 70% casein. Feeding 70% casein significantly stimulated increases of 32, 87, 74, 216, and 1,450% in pancreatic DNA, RNA, wet weight, protein content, and chymotrypsin content, respectively. Midcourse treatment with MK-329 was more effective than day zero treatment, and it completely reversed increases in pancreatic weight and RNA content, partially reversed increases in protein and chymotrypsin content, and had no effect on DNA content. Return to 5% casein rapidly reversed increases in pancreatic parameters, except for DNA. The results indicate that CCK is essential for induction and maintenance of dietary protein-stimulated pancreatic hypertrophy.

THU0072 Gastrin-Releasing Peptide (GRP) and RC-3095, a GRP Receptor Antagonist, Regulates Arthritic Mice Synovial Fibroblasts

2015 ◽  
Vol 74 (Suppl 2) ◽  
pp. 218.1-218
Author(s):  
V.S. Clarimundo ◽  
M. Farinon ◽  
C. Nör ◽  
L.I. Filipin ◽  
P.S. Gulko ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Synovial Fibroblasts ◽  
Gastrin Releasing Peptide ◽  
Grp Receptor

scholarly journals In Vivo Stabilization of a Gastrin-Releasing Peptide Receptor Antagonist Enhances PET Imaging and Radionuclide Therapy of Prostate Cancer in Preclinical Studies

Theranostics ◽  
2016 ◽  
Vol 6 (1) ◽  
pp. 104-117 ◽  
Author(s):  
Kristell L.S. Chatalic ◽  
Mark Konijnenberg ◽  
Julie Nonnekens ◽  
Erik de Blois ◽  
Sander Hoeben ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Receptor Antagonist ◽  
Pet Imaging ◽  
Radionuclide Therapy ◽  
Preclinical Studies ◽  
Peptide Receptor ◽  
Gastrin Releasing Peptide

A gastrin-releasing peptide receptor antagonist blocks d-amphetamine-induced hyperlocomotion and increases hippocampal NGF and BDNF levels in rats

Peptides ◽  
2007 ◽  
Vol 28 (7) ◽  
pp. 1447-1452 ◽  
Author(s):  
Márcia Kauer-Sant’Anna ◽  
Ana Cristina Andreazza ◽  
Samira S. Valvassori ◽  
Márcio Rodrigo Martins ◽  
Luciana M. Barbosa ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Peptide Receptor ◽  
Gastrin Releasing Peptide

Synthesis, radiolabeling, and evaluation of gastrin releasing peptide receptor antagonist 68 Ga-HBED-CC-RM26

2019 ◽  
Vol 62 (12) ◽  
pp. 843-849
Author(s):  
Drishty Satpati ◽  
Kusum Vats ◽  
Rohit Sharma ◽  
Mythili Kameswaran ◽  
Haladhar Dev Sarma ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Peptide Receptor ◽  
Gastrin Releasing Peptide

Preclinical and first clinical experience with the gastrin-releasing peptide receptor-antagonist [68Ga]SB3 and PET/CT

2015 ◽  
Vol 43 (5) ◽  
pp. 964-973 ◽  
Author(s):  
Theodosia Maina ◽  
Hendrik Bergsma ◽  
Harshad R. Kulkarni ◽  
Dirk Mueller ◽  
David Charalambidis ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Clinical Experience ◽  
Peptide Receptor ◽  
Gastrin Releasing Peptide ◽  
Pet Ct

scholarly journals Roles for substance P and gastrin-releasing peptide as neurotransmitters released by primary afferent pruriceptors

2013 ◽  
Vol 109 (3) ◽  
pp. 742-748 ◽  
Author(s):  
Tasuku Akiyama ◽  
Mitsutoshi Tominaga ◽  
Auva Davoodi ◽  
Masaki Nagamine ◽  
Kevin Blansit ◽  
...  
Keyword(s):  
Substance P ◽  
Receptor Antagonist ◽  
Sensory Neurons ◽  
Intrathecal Administration ◽  
Primary Sensory Neurons ◽  
Gastrin Releasing Peptide ◽  
Behavioral Studies ◽  
Neurokinin 1 ◽  
Protease Activated Receptor 2 ◽  
Grp Receptor

Recent studies support roles for neurokinin-1 (NK-1) and gastrin-releasing peptide (GRP) receptor-expressing spinal neurons in itch. We presently investigated expression of substance P (SP) and GRP in pruritogen-responsive primary sensory neurons and roles for these neuropeptides in itch signaling. Responses of dorsal root ganglion (DRG) cells to various pruritogens were observed by calcium imaging. DRG cells were then processed for SP, GRP, and isolectin B-4 (IB4; a marker for nonpeptidergic neurons) immunofluorescence. Of pruritogen-responsive DRG cells, 11.8–26.8%, 21.8–40.0%, and 21.4–26.8% were immunopositive for SP, GRP, and IB4, respectively. In behavioral studies, both systemic and intrathecal administration of a NK-1 receptor antagonist significantly attenuated scratching evoked by chloroquine and a protease-activated receptor 2 agonist, SLIGRL, but not histamine, bovine adrenal medulla peptide 8-22 (BAM8-22), or serotonin. Systemic or intrathecal administration of a GRP receptor antagonist attenuated scratching evoked by chloroquine and SLIGRL but not BAM8-22 or histamine. The GRP receptor antagonist enhanced scratching evoked by serotonin. These results indicate that SP and GRP expressed in primary sensory neurons are partially involved as neurotransmitters in histamine-independent itch signaling from the skin to the spinal cord.

Sign in / Sign up

Export Citation Format

Share Document