Abstract:
BACKGROUND:Adenosine released by cells during ischemia typically serves as a feedback inhibitor of further organ work. However, in ischemic intestine, adenosine appears to act via stimulatory A2b receptors to increase work in the form of chloride ion (Cl-) secretion. This unusual response may contribute to luminal fluid sequestration in intestinal ischemia. In nonischemic cells feed-forward activation of Cl- secretion does not occur despite the fact that adenosine may be continuously generated during normal cell metabolism. Thus we postulated that intestinal epithelia normally control the disposition of adenosine to prevent inappropriate activation of secretion. METHODS:Model T84 intestinal epithelia were studied by means of electrophysiologic and isotopic techniques. RESULTS:Dipyridamole and nitrobenzylthioinosine (inhibitors of nucleoside transport) and iodotubercidin (an inhibitor of adenosine kinase) caused adenosine to accumulate extracellularly and induced a Cl- secretory response that was prevented by adenosine receptor blockade. Uptake of exogenous adenosine was restricted to the basolateral compartment and was blocked by nucleoside transport inhibitors. CONCLUSIONS:Adenosine released from nonischemic intestinal epithelial cells is scavenged by a basolaterally restricted adenosine transporter. This system maintains extracellular adenosine levels below the prosecretory threshold and thus limits adenosine-elicited activation of Cl- secretion (and hence diarrhea) under normal conditions).
journal_name
Surgeryjournal_title
Surgeryauthors
Tally KJ,Hrnjez BJ,Smith JA,Mun EC,Matthews JBdoi
10.1016/s0039-6060(96)80295-9subject
Has Abstractpub_date
1996-08-01 00:00:00pages
248-54issue
2eissn
0039-6060issn
1532-7361pii
S0039-6060(96)80295-9journal_volume
120pub_type
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