Epithelia such as the renal proximal tubule reasorb fluid "isotonically" by osmotic coupling to active salt transport. This coupling has a rectifying character which means that solute accumulation on the basolateral side induces higher flow rates than the same accumulation on the apical side (for example, see [9]) and that small rises of hydrostatic pressure on the basolateral side reduce the fluid transport to almost zero but have very little effect from the apical side (for example, see [14]). These phenomena are usually related to the "leakiness" of the basolateral spaces [4], which are believed to be rendered hyperosmotic by the active salt transport and thus be the site where the coupling of salt and fluxes occurs [2]. It has been argued that a pressure gradient opposing the outflow of resorbate from these spaces to the interstitium may result in trapping of solutes and fluid so that the backleak of resorbate through the tight junctions rises and a higher fraction of the accumulated solutes is lost by diffusion from the basolateral spaces into the interstitium [19, 201. For the renal proximal tubule this concept has not only been used to explain rectification and isotonicity of the tubular fluid transport but also the dependency of fluid transport rate on the rate of glomerular filtration [17]. It has been argued that variation of glomerular l~tration rate with its concomitant variations of peritubular blood flow are reflected in appropriate variations of the renal interstitial hydrostatic pressure, which may finally adjust the tubular fluid transport rate to the rate of glomerular filtration by the above mechanism. However, apart from the fact that variations of glomerlar filtration do not induce significant alterations of the peritubular hydrostatic pressure [11], the original concept itself has come under challange through a variety of recent observations. For instance, it was found that water pemeates leaky epithelia predominantly through the cells [18]. In addition, a reinvestigation of the reflection coefficients for Na + and C1in isolated rabbit tubules in vitro found values a good deal closer to I than was originally the case [2, 6, 10]. Furthermore, many obervations on tight epithelia suggest that osmotic or hydrostatic pressure gradients across the epithelium may alter the cellular transport activity directly by unknown mechanisms localized within the cells themselves (for literature see [12]). This seems also to be true for leaky epithelia since, for example, when hydrostatic pressure on the basolateral side of gallbladders is raised, the undirectional sodium flux from the apical to the basolateral side is diminished whereas the opposing flux is only minimally increased [7]. Similarly, the addition of