Bile Acids and the Intestinal Kallikrein-Kinin System
We have measured concentrations of tissue kallikrein-like amidase (TKLA) in blood-free rat gastrointestinal tissue. TKLA was present in the gut wall from the stomach to the rectum with concentration peaks in the duodenum and caecum. When rats, fasted for 24 hr were compared with normally fed animals, the mean fasted TKLA levels rose significantly in the duodenum and proximal and distal colons and fell in the caecum. No other tissues showed concentration changes.
Sodium chenodeoxycholate and other bile acids have biological actions on the rat intestinal wall which are similar to those produced by the kallikrein-kinin system. We have previously reported that bile acids released TKLA from the rat colon wall. This TKLA was totally inhibited by aprotinin.
We now report that intraluminal sodium chenodeoxycholate (30 mM) increases both colonic motility and colonic mucosal leakage. These increases are largely blocked by aprotinin.
The ability of intraluminal sodium taurochenodeoxycholate to increase vascular leakage in the rat stomach and colon was parallelled by its ability to release TKLA from these issues.
Our results are compatible with the mediation of these biological actions of the tested bile acids via activation of a serine proteinase, possibly tissue kallikrein.
KeywordsBile Acid Bile Salt Vascular Leakage Krebs Solution Colonic Motility
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