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Am J Physiol Gastrointest Liver Physiol (August 7, 2002). doi:10.1152/ajpgi.00193.2002
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Articles in PresS, published online ahead of print August 7, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00193.2002
Submitted on May 21, 2002
Accepted on July 30, 2002

Uncoupling Protein-1 (UCP1): involvement in a novel pathway for ß-adrenergic, cAMP-mediated intestinal relaxation

Irina Shabalina1, Claes Wiklund2, Tore Bengtsson1, Anders Jacobsson1, Barbara Cannon1, and Jan Nedergaard1*

1 The Arrhenius Laboratories F3, Stockholm University, The Wenner-Gren Institute, Stockholm, Sweden
2 Department of Anaesthesiology and Intensive Care Medicine, Karolinska Hospital and Institute, Stockholm, Sweden

* To whom correspondence should be addressed. E-mail: jan{at}metabol.su.se.

The pathway for adrenergic relaxation of smooth muscle is not fully understood. As UCP1 (mitochondrial uncoupling-protein-1) expression occurs in cells within the longitudinal smooth muscle layer of organs exhibiting peristalsis, we examined whether the absence of UCP1 affects adrenergic responsiveness. Intestinal (ileal) segments were obtained from UCP1-ablated and from wild-type mice (C57Bl/6, 129/SvPas and outbred NMRI). In UCP1-containing mice, isoprenaline totally inhibited contractions induced by electrical field stimulation, but in intestine from UCP1-ablated mice, a significant residual contraction remained even at high isoprenaline concentrations; the segments were 3-fold less sensitive. Also when contraction was induced by carbachol, there was a residual isoprenaline-insensitive contraction. Similar results were obtained with the ß3-selective agonist CL-316,243 and with the adenylyl cyclase stimulator forskolin. Thus, the UCP1 expressed in the longitudinal muscle layer of the mouse intestine is apparently functional; UCP1, presumably through uncoupling, may be involved in a novel pathway leading from increased cAMP levels to relaxation in organs exhibiting peristalsis.




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