No abstract

Earlier we demonstrated significant differences in proximal tubular Na transport inhibition during saline volume expansion (VE) depending on whether artificial (AF) or native harvested tubular fluid (HTF) was used. In the present experiments the shrinking-drop technique was used to measure volume flux (Jv) in the early- and late-clip models of VE with AF alternating with HTF. In early-clip rats, with AF, Jv (x 10(4) mm3.mm-2.s-1) during the nonexpanded period was 2.92 +/- 0.105; during subsequent VE, it was 2.20 +/- 0.180 and 1.97 +/- 0.149 with HTF (for the latter two P greater than 0.3). In late-clip rats they were 2.83 +/- 0.135, 1.99 +/- 0.157, and 1.50 +/- 0.171 (for the latter two P less than 0.001), respectively. With AF, transport was inhibited equally in both models during VE. There were no significant differences in the electrolyte composition of AF and HTF during shrinkage as measured by microprobe analysis. The 47% inhibition of Jv with HTF but not AF during VE in the late-clip but not the early-clip rats strongly implies the presence of factors other than physical forces during VE, which inhibit proximal tubular Na transport. Studies of tubular transport during VE need to be performed using both AF and HTF.

In dual micropuncture experiments the shrinking drop technique was used to measure volume flux with artificial tubular fluid (AF) alternating with harvested tubular fluid (HTF) during saline volume-expanded (VE) and nonexpanded (NE) periods. In VE rats, volume flux (Jv) (nl.mm-1.min-1) with AF was 1.78 +/- 0.08 (means +/- SE) during NE and was reduced to 1.39 +/- 0.09 (P = 0.01) during subsequent VE, whereas with randomly alternating HTF during VE it was 1.07 +/- 0.08 (P less than 0.0001 and less than 0.03, respectively). Jv with HTF from NE rats tested in the VE rats was 1.20 +/- 0.06, which is significantly higher than that measured with their own HTF (Wilcoxon rank, P = 0.05). In NE rats Jv was 1.65 +/- 0.10 and 1.69 +/- 0.10 with AF and HTF and was 1.28 +/- 0.07 (P less than 0.001 from both) with HTF obtained from VE rats. Elemental analysis of reaspirated tubular fluids showed no significant differences in Na or Cl concentrations among any of the fluids. It is concluded that during VE, a transferable Na transport inhibitor appears in proximal tubular fluid, which, together with a changed proximal tubular epithelium, possibly due to physical forces, accounts for proximal tubular Na transport inhibition during VE.

To investigate whether atrial natriuretic peptides (ANP) are entirely responsible for the natriuresis of volume expansion (VE), we studied the natriuresis from acutely snared and nonsnared kidneys of rats undergoing sustained saline VE and subsequent infusion of maximal doses of ANP (atriopeptin II), or vice versa. Fractional excretion of Na (FENa) was increased from control (0.15 +/- 0.03%) to 4.6 +/- 0.6% by VE and to 10.9 +/- 1.5% by subsequent ANP infusion. With ANP alone FENa increased from control (0.24 +/- 0.04%) to 2.6 +/- 0.3%, and to 10.8 +/- 0.9% with VE, showing additive effects by both. Natriuresis with VE was significantly greater than with ANP alone (P less than 0.01) and both exhibited synergism, producing significantly greater natriuresis in the presence of the other than alone (P less than 0.05 for both). A reduction in perfusion pressure inhibited the effects of ANP and reduced that of VE. Natriuresis was produced by ANP independently of changes in glomerular filtration rate. It is concluded that 1) VE and ANP produce natriuresis by different renal mechanisms and that therefore, ANP can only account for part of the natriuresis of sustained VE; 2) the two have a synergistic interaction on natriuresis, probably through an intrarenal mechanism.