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

Abstract

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.

Melatonin inhibits alcohol-induced increases in duodenal mucosal permeability in rats in vivo

“…Furthermore, it has previously been shown that nicotinic receptor blockade almost abolish the hypotonicity-induced increase in mucosal permeability (32) but not that induced by acid or ethanol as shown in the present study (15). These data suggest that the increase in duodenal epithelial permeability in response to ethanol, acid, or hypotonicity is mediated by different mechanisms supporting the notion of physiological regulation of duodenal epithelial paracellular permeability.…”

Products of cyclooxygenase‐2 depress duodenal function in rats subjected to abdominal surgery

“…Another positive action of COX inhibition is the increase in mucosal 'protective' bicarbonate secretion, an effect most probably coupled to the induction of duodenal motility (Sababi & Nylander 1994, Sababi et al 1996, Nylander et al 2001. This effect in turn may be coupled to the increase in mucosal permeability and net fluid absorption seen after COX-inhibition (Nylander et al 2003). This effect in turn may be coupled to the increase in mucosal permeability and net fluid absorption seen after COX-inhibition (Nylander et al 2003).…”

Comparative study of the effect of luminal hypotonicity on mucosal permeability in rat upper gastrointestinal tract

“…Interestingly, perfusion of the duodenum with hypotonic solutions increases the bloodto-lumen clearance of 51 Cr-EDTA, a reliable probe for assessment of paracellular permeability in vivo (Nylander & Hä llgren 1998), in an osmolality-dependent manner, i.e. The physiological function of the hypotonicityinduced increase in permeability may be to 'boost' the transfer of osmolytes, mainly NaCl, into the lumen thereby facilitating the adjustment of luminal osmolality (Nylander et al 2003). Furthermore, there exists a strong positive linear correlation between the increase in mucosal permeability and the rise in luminal osmolality.…”