Submitted on April 17, 2003
Accepted on December 15, 2003
Involvement of Mast Cells in Basal and Neurotensin-induced Intestinal Absorption of Taurocholate in Rats
Xianyong Gui1 and Robert E. Carraway1*
1 Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA
* To whom correspondence should be addressed. E-mail: Robert.Carraway{at}umassmed.edu.
Neurotensin (NT), a hormone released from intestine by ingested fat, facilitates lipid
digestion by stimulating pancreatic secretion and slowing the movement of chyme. In
addition, NT can contract the gall bladder and enhance the enterohepatic circulation of bile
acids (EHC) to promote micelle formation. Our recent finding that NT enhanced and NT
antagonist inhibited 3H-taurocholate (3H-TC) absorption from proximal rat small intestine
indicated a role for endogenous NT in the regulation of EHC. Here, we postulate the
involvement of intestinal mast cells in the TC uptake process and in the stimulatory effect of
NT. In anesthetized rats with the bile duct cannulated for bile collection, infusion of NT (10
pmol/kg/min) enhanced the 3H-TC recovery rate from duodenojejunum by 2.2-fold. This
response was abolished by pretreatment with mast cell stabilizers (cromoglycate,
doxantrazole) and inhibitors of mast cell mediators (diphenhydramine, metergoline, zileuton).
In contrast, mast cell degranulators (compound 48/80, substance P) and mast cell mediators
(histamine, LTC4) reproduced the effect of NT. L-NAME enhanced and L-arginine inhibited
basal and NT-induced TC uptake, consistent with the known inhibitory effect of NO on mast
cell reactivity. These results argue that basal and NT-stimulated TC uptake in rat jejunum are
similarly dependent on mast cells, are largely mediated by release of mast cell mediators and
are subject to regulation by NO.
