Pressure control of sodium reabsorption and intercellular backflux across proximal kidney tubule.

The magnitude of changes in luminal hydrostatic pressure (DeltaP(L)), peritubular capillary hydrostatic pressure (DeltaP(PT)), and peritubular capillary colloid osmotic pressure (Deltapi) was determined in the Necturus kidney during volume expansion (VE). The specific effects of separate changes of each pressure parameter on proximal net sodium transport (J(Na)) were studied in isolated perfused kidneys. The combined effect of DeltaP(L), DeltaP(PT), and Deltapi, of a magnitude similar to that induced by volume expansion, decreases J(Na) by 26% in the perfused kidney. A major portion of the natriuresis in VE is due to changes in intrarenal pressures. The effect of Deltapi on the permeability characteristics of Necturus proximal tubule was studied. With increasing Deltapi, the ionic conductance of the paracellular shunt pathway decreased, since transepithelial input and specific resistance rose significantly, whereas cellular membrane resistance remained unchanged. Transepithelial permeability coefficients for sodium chloride and raffinose changed inversely proportional to transepithelial resistance, indicating an alteration of a paracellular permeation route. Net passive sodium backflux and active transport flux components were calculated. Increased net sodium transport with rising Deltapi is accompanied by a significant drop in passive back diffusion, without an increment in the active flux component. Change in passive sodium ion back diffusion thus appears to be a key physiological factor in the control of transepithelial sodium transport.