Abstract
The duodenal mucosa is regularly exposed to a low osmolality, and recent experiments suggest that hypotonicity increases mucosal permeability in an osmolality-dependent manner. The aim was to examine whether the sympathetic nervous system, via action on α-adrenoceptors, affects the hypotonicity-induced increase in duodenal mucosal permeability. The duodenum of anaesthetised rats was perfused in vivo with a 50 mM NaCl solution in the presence of adrenergic α-adrenoceptor drugs. Studied were the effects on mucosal permeability (blood-to-lumen clearance of 51Cr-EDTA), arterial blood pressure, luminal alkalinisation, transepithelial fluid flux, and motility. Hypotonicity induced a six-fold increase in mucosal permeability, a response that was reversible and repeatable. The α2-adrenoceptor agonist clonidine abolished the hypotonicity-induced increase in mucosal permeability, reduced arterial blood pressure, inhibited duodenal motility, and decreased luminal alkalinisation. The α2-adrenoceptor antagonists, yohimbine and idazoxan, prevented the inhibitory effect of clonidine on the hypotonicity-induced increase in mucosal permeability. The α1-agonist phenylephrine or the α1-antagonist prazosin elicited their predicted effect on blood pressure but did not affect the hypotonicity-induced increase in mucosal permeability. None of the α1- or α2-adrenoceptor drugs changed the hypotonicity-induced net fluid absorption. In conclusion, stimulation of the adrenergic α2-adrenoceptor prevents the hypotonicity-induced increase in mucosal permeability, suggesting that the sympathetic nervous system has the capability to regulate duodenal mucosal permeability.
Highlights
When an individual drinks water, coffee, diet soda, or tea on an empty stomach, the duodenal mucosa will be exposed to a fluid osmolality considerably lower than in blood plasma
The 100 mOsm-induced net increase in permeability in lidocaine treated rats was the same as that induced by pure water [1]. These results strongly suggests that the hypotonicity-induced increase in duodenal mucosal permeability is physiologically regulated
The major aim of the present investigation was to elucidate whether α-adrenergic receptor agonists and antagonists affect the hypotonicity-induced increase in duodenal mucosal permeability
Summary
When an individual drinks water, coffee, diet soda, or tea on an empty stomach, the duodenal mucosa will be exposed to a fluid osmolality considerably lower than in blood plasma. The low luminal osmolality induces water absorption and increases the efflux of osmolytes, which combined increase luminal osmolality. These transport processes have long been considered to occur passively across the “leaky” duodenal epithelium, by means of osmosis and solute diffusion. In 2003, Nylander and coworkers [1] demonstrated that perfusion of the duodenum with hypotonic solutions increased, in an osmolality-dependent manner, the blood-to-lumen clearance of chromium-51 labeled ethylenediamine tetraacetic acid (51 Cr-EDTA), despite the presence of a marked net water absorption. Additional experiments revealed that luminal hypotonicity increases the blood-to-lumen clearance of 14 C-methylglucose and 14 C-inulin, implicating increases in epithelial paracellular permeability [2]. The hypotonicity-induced increase in mucosal permeability showed to be fully reversible within 20 min after cessation of the hypotonic perfusion, supporting the view of a physiological response
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