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MUCOSAL BIOLOGY

Hypotonicity-induced increases in duodenal mucosal permeability facilitates adjustment of luminal osmolality

¹Department of Neuroscience, Division of Physiology, Biomedical Center, Uppsala University, S-751 23 Uppsala, Sweden; and ²School of Physiology and Pharmacology, University of New South Wales, Sydney 2052, Australia

Submitted 4 October 2002 ; accepted in final form 2 April 2003

The integrated response to hypotonic NaCl solutions (100, 50, 25, and 0 mM NaCl) in proximal duodenum of anesthetized rats was examined. Luminal alkalinization, fluid flux, duodenal contractions, blood-to-lumen clearance of ⁵¹Cr-labeled EDTA (mucosal permeability), and perfusate osmolality were studied in the absence and presence of the cyclooxygenase inhibitor indomethacin. In response to hypotonic solutions net fluid absorption, increases in permeability and perfusate osmolality were markedly higher in indomethacin-treated animals than in controls, and these effects were diminished by the nicotinic-receptor antagonist hexamethonium. Infusion of iloprost, a stable PGI₂ analog, to indomethacin-treated animals markedly reduced the hypotonicity-induced increase in mucosal permeability and diminished the rise in perfusate osmolality. Lowering the NaCl concentration in the perfusion solution but maintaining isotonicity with mannitol had no effect on mucosal permeability. Very good linear correlations were obtained between the degree of luminal hypotonicity and the increase in permeability and between increases in permeability and perfusate osmolality. It is concluded that luminal hypotonicity increases duodenal mucosal permeability. The hypotonicity-induced increase in permeability modulated by prostaglandins and nicotinic receptors fulfills the function of increasing blood-to-lumen transport of Na⁺ facilitating adjustment of luminal osmolality.

absorption; ⁵¹Cr-labeled EDTA; cyclooxygenase; motility; secretion

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