Luminal adenosine stimulates chloride secretion through A 1 receptor in mouse jejunum

• Published in: American journal of physiology: Gastrointestinal and liver physiology Vol. 288; no. 5; pp. G972 - G977
• Main Authors: Ghanem, Esam, Lövdahl, Cecilia, Daré, Elisabetta, Ledent, Catherine, Fredholm, Bertil B., Boeynaems, Jean-Marie, Van Driessche, Willy, Beauwens, Renaud
• Format: Journal Article
• Language: English
• Published: 01.05.2005
• ISSN: 0193-1857; 1522-1547
• DOI: 10.1152/ajpgi.00346.2004

Adenosine is known to stimulate chloride secretion by mouse jejunum. Whereas the receptor on the basolateral side is believed to be A 2B , the receptor involved in the luminal effect of adenosine has not been identified. We found that jejuna expressed mRNA for all adenosine receptor subtypes. In this study, we investigated the stimulation of chloride secretion by adenosine in jejuna derived from mice lacking the adenosine receptors of A 1 (A 1 R) and A 2A (A 2A R) or control littermates. The jejunal epithelium was mounted in a Ussing chamber, and a new method on the basis of impedance analysis was used to calculate the short-circuit current ( I sc ) values. Chloride secretion was assessed by the I sc after inhibition of the sodium-glucose cotransporter by adding phloridzin to the apical bathing solution. The effect of apical adenosine on chloride secretion was lost in jejuna from mice lacking the A 1 R. There was no difference in the response to basolaterally applied adenosine or to apical forskolin. Furthermore, in jejuna from control mice, the effect of apical adenosine was also abolished in the presence of 8-cyclopentyl-1,3-dipropylxanthine, a specific A 1 R antagonist. Responses to adenosine were identical in jejuna from control and A 2A R knockout mice. This study demonstrates that A 1 R (and not A 2A R) mediates the enhancement of chloride secretion induced by luminal adenosine in mice jejunum.