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Prokineticin 1 inhibits spontaneous giant contractions in the murine proximal colon through nitric oxide release
Author(s) -
Hoogerwerf W. A.
Publication year - 2006
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/j.1365-2982.2006.00776.x
Subject(s) - nitric oxide , nitric oxide synthase , myenteric plexus , contractility , interstitial cell of cajal , enteric nervous system , medicine , endocrinology , inhibitory postsynaptic potential , receptor , biology , microbiology and biotechnology , motility , chemistry , biochemistry , smooth muscle , immunohistochemistry
Prokineticins are novel peptides with reported effects on gastrointestinal contractility. Prokineticin actions are mediated by distinct prokineticin receptors (PKR1 and PKR2). This study investigated the role of prokineticin 1 in colonic contractility as well as sites of expression of its receptor in the mouse proximal colon by immunohistochemistry and confocal microscopy. Prokineticin 1 suppressed giant contractions in circular muscle. The inhibitory effect of prokineticin 1 on giant contractions was blocked by the nitric oxide synthase (NOS) inhibitor N (omega)‐nitro‐ l ‐arginine methyl ester ( l ‐NAME). In vitro , prokineticin 1 stimulated nitric oxide release from longitudinal muscle‐myenteric plexus cultures. This effect was blocked by l ‐NAME. PKR1 is expressed on myenteric plexus neurons and colocalizes with a small subset of nNOS expressing neurons. This study suggests that PKR1 mediates an inhibitory effect in vitro , most likely through direct or indirect stimulation of nitric oxide release. PKR1 and its natural ligand, prokineticin 1 may be important for modulation of colonic motility.