Water transport revisited

Nearly forty years ago Curran Naftalin & Pedley, 1999) in this issue of TheThe Journal of Physiology shed light on this question by proposing a role for the myofibroblast-reticular sheath (which they call the fibronexus). This ‘sheath’ forms a second fenestrated ‘membrane’ just under the fenestrated BM in the intestine and probably most epithelial tissues (Toyoda et al. 1997). Heretofore, this myofibroblastic syncytium had been thought only to influence intestinal secretion through prostaglandin (cyclic AMP)-mediated sensitization of intestinal epithelial cells to Ca2+-mediated secretogogues (Berschneider & Powell, 1992). Using confocal microscopy to identify this ‘sheath’ and a fluorescent probe for Na+, these investigators show that it presents a diffusion barrier to Na+ that correlates well with the gut segments that are able to transport hypertonically. These experiments suggest that the reflection coefficient of the BM is such that this barrier is adequate for isotonic transport, but that the myofibroblast-reticular sheath serves as an additional diffusion barrier in series with the BM in order to accomplish hypertonic transport. Alternatively, it may be that it is the myofibroblast-reticular sheath, and not the BM, which represents the basolateral diffusion barrier for either isotonic or hypertonic transport. The investigators have also shown a correlation between the barrier function of this sheath and a high renin-angiotensin II-aldosterone state brought about by dietary Na+ depletion. It has been previously known that such a state greatly increases distal colonic Na+ transport by increasing the resistance of the tight junctions and by increasing expression of amiloride-sensitive Na+ channels and Na+,K+-ATPase on the apical and basolateral membranes of the distal colonocyte. Naftalin and colleagues propose that this sodium depletion state also leads to greater osmotic transport, through angiotensin II- or aldosterone-induced activation of the myofibroblasts with increased synthesis and secretion of reticulin fibrils, resulting in changes in the reflection coefficient of this myofibroblast-reticular membrane. These investigators give increased verification and clearer biological counterparts to a model of transport proposed nearly half a century ago. It remains to be determined if this myofibroblast-reticular sheath has such a transport function in all electrolyte and water transporting epithelia. It appears that the syncytium of myofibroblasts exists under the epithelial BM in all transporting epithelia where it has contractile functions and growth, differentiation and wound repair functions. This syncytium will be the subject of considerable investigation over the next few years.