Effects of a small serosal hydrostatic pressure on sodium and water transport and morphology in rabbit gall-bladder

1. In order to investigate the mechanism of serosal pressure-induced inhibition of isosmotic fluid transport, the effect of 4.5 cm water serosal pressure on spontaneous water transfer (J(v)) in rabbit gall-bladders was measured (in the presence of a supporting soft nylon net on the mucosal side) in a modified Ussing chamber. This allowed unidirectional Na(+) fluxes ([Formula: see text] and [Formula: see text]), transepithelial potential difference and resistance (R(t)) to be measured simultaneously. The effects of the serosal pressure were also investigated by light and electron microscopy.2. During pressure application, R(t) increased due to a covering effect of the mucosal support. The serosal pressure caused a parallel decrease in J(v) and net Na(+) transport ([Formula: see text]) across the free epithelial surface of 80-85%. About 85% of the decrease in [Formula: see text] was due to a decrease in [Formula: see text].3. After inhibition of 93% of fluid absorption by serosal 10(-3)M-ouabain, pressure-induced change in J(v) was only 8% of the spontaneous fluid transport rate.4. Control Na(+) flux ratio ([Formula: see text]) was 3.5. The pressure-induced increase in steady-state [Formula: see text] of 30-35% therefore contributed little to the decrease in [Formula: see text]. Further, this increase in [Formula: see text] was completely prevented by mucosal 10(-3) M-amiloride.5. All pressure-induced effects on transport and electrical parameters were reversible.6. The light microscopical and scanning electron microscopical results showed that half of the epithelial surface was covered by the nylon net following serosal pressure application. Ruptures in the epithelium were not seen. Thin section and freeze fracture electron microscopy demonstrated continuous, well developed tight junctions both in control and experimental condition.7. It is concluded that a serosal pressure of only 4.5 cm water causes inhibition of a cellular active Na(+) and water transport with only minimal, if any, contribution from paracellular filtration. This would seem incompatible with the concept that an active ion transport mechanism localized in the basolateral cell membrane is responsible for transepithelial fluid transport. The possibility of a mechanical fluid transport mechanism via elements of a tubulo-cisternal endoplasmic reticulum is raised.