Background/aim: This study addresses cholecystokinin (CCK)-receptor alterations in stone-diseased and stone-free human gallbladders using different CCK-fragments.
Methods: Serosa-free muscle strips were mounted in a modified Krebs-Henseleit-solution of 37 degrees C and aerated with carbogen. The following concentrations of CCK-fragments (CCK 26-33, N-Acetyl CCK 27-33 sulf., CCK 26-29 sulf., CCK 25-33 sulf.) were achieved: 0.1 nmol, 0.5 nmol, 2 nmol, 10 nmol, 100 nmol.
Results: Stone-diseased gallbladders were classified into two groups based on their in vitro reaction to CCK 26-33 (CCK-octapeptide). Muscle strips not contracting below 10 nmol were assigned to the subcontractor group. Histologically scarification, necrosis and signs of severe inflammation of the mucosa were seen in 76.9% of this group. Those starting contractions at 0.1 nmol (like the control group) were called the contractor group. This group had a shallow mucosa and mild inflammatory signs in 54.5%. The sub-contractor group showed higher spontaneous phasic activity at lower tonic activity than the contractor and control groups. In the sub-contractor group CCK 27-33 caused several times higher contractions than all other fragments. A maximal contraction level in the contractor and control groups was reached by CCK 25-33.
Conclusions: This striking effect of CCK 27-33 in the sub-contractor group favors the view of CCK-receptor structural alteration in a subgroup of patients with cholecystolithiasis.
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http://dx.doi.org/10.1016/s0168-8278(97)80115-8 | DOI Listing |
Biochem Biophys Res Commun
February 2004
Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Key amino acids of the cholecystokinin (CCK) peptide for receptor binding are sulfated Y27, W30, D32, and F33-NH(2). Three-dimensional modeling showed that the CCK-A receptor (CCK-AR) antagonist devazepide penetrated into the transmembrane (TM) domains, whereas CCK was placed on the surface of the CCK-AR. Four types of rat CCK-AR cDNAs were transfected into CHO-K1 and COS-7 cells: normal CCK-AR cDNA transfected cells (wild type, WT); K120 substituted with V; K130V; and R352V.
View Article and Find Full Text PDFAm J Physiol
December 1997
Institut National de la Santé et de la Recherche Médicale Unité 30, Hôpital Necker-Enfants-Malades, Tour Lavoisier, Paris, France.
The tripeptide pyro-Glu-His-Pro-NH2[thyrotropin-releasing hormone (TRH)] was isolated from the hypothalamus as a thyrotropin-releasing factor. It has a broad spectrum of central nervous system-mediated actions, including the stimulation of exocrine pancreatic secretion. TRH is also synthesized in the endocrine pancreas and found in the systemic circulation.
View Article and Find Full Text PDFJ Hepatol
May 1997
Department of General Surgery, Johann Wolfgang Goethe-University, Frankfurt/Main, Germany.
Background/aim: This study addresses cholecystokinin (CCK)-receptor alterations in stone-diseased and stone-free human gallbladders using different CCK-fragments.
Methods: Serosa-free muscle strips were mounted in a modified Krebs-Henseleit-solution of 37 degrees C and aerated with carbogen. The following concentrations of CCK-fragments (CCK 26-33, N-Acetyl CCK 27-33 sulf.
J Pharmacol Exp Ther
December 1994
Département de Pharmacochimie Moléculaire et Structurale, U266 Institut National de la Santé et de la Recherche Médicale, Paris, France.
Published results suggest that delta-opioid agonists can modulate the mu-mediated analgesia. In this work, the antinociceptive effects produced by the mu agonist [D-Ala2,NMe-Phe4,Gly-ol5]enkephalin or the mixed inhibitor of enkephalin-degrading enzymes RB 101 (N- [(R,S)-2-benzyl-3[(S)(2-amino-4-methyl- thio)butyldithio]-1-oxopropyl]-L-phenylalanine benzyl ester) were studied after administration of the systemically active and selective delta agonist Tyr-D-Ser(O-tert-butyl)-Gly-Phe-Leu- Thr(O-tert-butyl). In the hot-plate test in mice, Tyr-D-Ser(O-tert-butyl)-Gly- Phe-Leu-Thr(O-tert-butyl) (i.
View Article and Find Full Text PDFNeurosci Lett
October 1993
Unité de Pharmacochimie Moléculaire et Structurale, U 266 INSERM-URA 1500 CNRS, Université René Descartes, UFR des Sciences Pharmaceutiques et Biologiques, Paris, France.
The effects of intracerebroventricular administration of the cholecystokinin (CCK) analogue, BDNL, and the selective CCK-B agonist, BC 264, were determined using the hot plate test in mice. BDNL (0.2 nmol and 0.
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