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1 Department of Cell Physiology, Free University of Brussels, Brussels, Belgium
2 Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
3 Institute of Interdisciplinary Research, Free University of Brussels, Brussels, Belgium
4 Institute of Interdisciplinary Research, Free University of Brussels, Brussels, Belgium; Department of Medical Chemistry, Erasme Hospital, Free University of Brussels, Brussels, Belgium
5 Department of Physiology, KU Leuven, Leuven, Belgium
* To whom correspondence should be addressed. E-mail: renbeau{at}ulb.ac.be.
Adenosine is known to stimulate chloride secretion by mouse jejunum. Whereas the receptor on the basolateral side is believed to be A2B, 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 A1 (A1R) and A2A (A2AR) or control littermates. The jejunal epithelium was mounted in an Ussing chamber and a new method based on impedance analysis was used to calculate the short-circuit current values. Chloride secretion was assessed by the short circuit current following 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 A1R. 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 presence of 8-cyclopentyl-1,3dipropylxanthine (DPCPX), a specific A1R antagonist. Responses to adenosine were identical in jejuna from control and A2AR knockout mice. This study demonstrates that A1R (and not A2AR) mediates the enhancement of chloride secretion induced by luminal adenosine in mice jejunum.
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