A submucosal mechanism for catecholamine‐induced increases in fluid absorption in rabbit ileum in vitro.

Abstract

SUMMARY1. The effects of clonidine and dopamine on water movements across the mucosal and serosal surfaces of rabbit ileum have been investigated using a high-resolution method for monitoring water flows in vitro.2. Theophylline (10 mM) and carbamyl choline (10 /1M) caused a reduction in fluid inflow across the mucosal surface and a smaller decrease in fluid outflow across the serosal surface. Addition of the x2-adrenergic agonist clonidine or dopamine fully reversed the theophylline, or carbamyl choline-induced decrease in mucosal inflow in a dose-related manner.3. The effects of clonidine on mucosal inflow are blocked by the a2-adrenergic antagonist, yohimbine. Yohimbine was much less effective than pimozide or dbutaclamol in blocking the effect of dopamine on mucosal inflow. These findings support the view that there are separate a2-adrenergic and dopaminergic receptors. Theophylline reduced the Lp by 35 %. Clonidine (1 ,UM) added to theophylline-treated tissues increased the Lp by 66%. This effect was prevented by yohimbine (1 uM).5. The effects of theophylline, clonidine and dopamine on the permeability of the mucosal and serosal surfaces of the tissue to [3H]mannitol were measured. These showed that theophylline increased the rate of labelled mannitol loss across the mucosal surface but reduced the mannitol permeability across the serosal surface. This latter effect was reversed by clonidine and dopamine.6. Changes in transepithelial electrical potential difference (PD), short-circuit current and resistance were monitored. Theophylline caused a rapid increase in PD and short-circuit current and a slower increase in resistance. Clonidine (5 /bM) reversed the effects on PD and resistance but was without significant effect on shortcircuit current. The results suggest that a major component of secretagogue-induced reduction in fluid transport in vitro is due to mechanical changes in the submucosa, probably induced by modulation of neurotransmitter release within the tissue.

A submucosal mechanism of action for prostaglandin E2 on hexose absorption and metabolism in mouse intestine.

“…This suggests that PGE2 may regulate hexose absorption and metabolism by influencing submucosal release of neurotransmitters from the enteric neural network. Spontaneously active neurons from the submucosal plexus are thought to have a direct or indirect inhibitory influence on the mucosa (Andres, Bock, Bridges, Rummel & Schreiner, 1985;Ahsan, Naftalin & Smith, 1988). Certainly, we observed that a-MG uptake by isolated epithelial cells in the present study was enhanced by carbachol and noradrenaline.…”

Evidence from fluorescence microscopy and comparative studies that rat, ovine and bovine colonic crypts are absorptive.

“…We have proposed that small intestinal fluid secretion in vitro is observed when net fluid outflow via intercellular junctions induced by interstitial hydrostatic pressure, exceeds the absorptive flow across the mucosal surface, induced by transcellular and transjunctional osmotic pressure (Ahsan, Ilundain, Naftalin, Sandhu & Smith 1987;Ahsan, Naftalin & Smith, 1988). The presence of a layer of contractile myofibroblasts immediately subjacent to colonic mucosal epithelium could generate this flow in colon (Joyce, Haire & Palade, 1987).…”

The Impact of α-Adrenoceptors in the Regulation of the Hypotonicity-Induced Increase in Duodenal Mucosal Permeability In Vivo

“…So, what is the mechanism by which clonidine inhibits the hypotonicity-induced increase in mucosal permeability? In a study by Ahsan et al [23], in isolated rabbit ileum, it was suggested that α 2 -agonists reduce interstitial fluid pressure by depressing smooth muscle tone. A decrease in interstitial fluid pressure may reduce the driving forces for the transport of 51 Cr-EDTA from interstitium-to-lumen.…”