These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Regulation of canine gallbladder motility by brain peptides.
    Author: Lenz HJ, Zimmerman FG, Messmer B.
    Journal: Gastroenterology; 1993 Jun; 104(6):1678-85. PubMed ID: 8500726.
    Abstract:
    BACKGROUND: Brain peptides alter most gastrointestinal functions, but their effects on gallbladder motility have not been examined in detail. METHODS: Studies were conducted in awake, male beagle dogs. RESULTS: Of 30 brain peptides evaluated, thyrotropin-releasing hormone (TRH) and calcitonin gene-related peptide (CGRP) inhibited CCK- and meal-induced gallbladder contraction. These responses were abolished by ganglionic blockade. Truncal vagotomy prevented the central inhibitory action of TRH but not that of CGRP, whereas noradrenergic blockade prevented the central inhibitory action of CGRP but not that of TRH. Muscarinic blockade did not prevent the relaxing effect of cerebral TRH but pretreatment with the vasoactive intestinal peptide (VIP) antagonist, (4Cl-D-Phe6-Leu17)VIP, significantly attenuated gallbladder relaxation induced by cerebral TRH: the combination of both VIP and muscarinic antagonists abolished TRH-induced gallbladder relaxation. alpha-Adrenergic receptor blockade but neither beta-adrenergic blockade nor adrenalectomy abolished gallbladder relaxation induced by cerebral CGRP. Intravenous infusion of VIP and norepinephrine inhibited CCK-induced gallbladder contraction and these responses were abolished dose dependently by intravenous infusion of (4Cl-D-Phe6-Leu17)VIP and phentolamine, respectively. CONCLUSIONS: Cerebral TRH inhibits canine gallbladder contraction by stimulation of vagal outflow and subsequent release of VIP acting via its specific receptor whereas cerebral CGRP inhibits gallbladder contraction by stimulation of sympathetic, noradrenergic outflow via alpha-adrenergic receptors.
    [Abstract] [Full Text] [Related] [New Search]