Proximal tubular cell electrolytes during volume expansion in the rat.

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RESUMO

1. Proximal tubular intracellular elements were measured by electron microprobe X-ray analysis (a) in rats volume-expanded with albumin-saline in which peritubular oncotic pressure remained normal and (b) in rats in which the renal artery was snared before volume expansion (the early snare model). Glomerular filtration rate and urine Na+ excretion were measured in addition to intracellular Rb+ following a 30 s infusion of RbCl as a marker for K+ transport. 2. In albumin-saline volume-expanded rats, intracellular levels of Na+ ([Na+]i) at 21.5 +/- 0.6 mmol (kg wet wt)-1, Cl- ([Cl-]i) at 18.0 +/- 0.4 mmol (kg wet wt)-1 and Rb+ ([Rb+]i) at 9.4 +/- 0.4 mmol (kg wet wt)-1 were significantly higher (P < 0.0001) than the levels in non-expanded rats ([Na+]i, [Cl-]i and [Rb+]i at 17.7 +/- 0.4, 14.6 +/- 0.3 and 4.7 +/- 0.4 mmol (kg wet wt)-1, respectively; means +/- S.E.M.). The data are consistent with Na+ pump inhibition in the proximal tubule, although this cannot be directly derived from intracellular element measurements. 3. In an early snare model of volume expansion, [Na+]i, intracellular K+ ([K+]i) and [Rb+]i remained unchanged (16.1 +/- 0.4, 131.0 +/- 2.0 and 5.2 +/- 0.3 mmol (kg wet wt)-1, respectively) compared to non-expanded snared kidneys (15.9 +/- 0.6, 131.3 +/- 1.8 and 4.8 +/- 0.3 mmol (kg wet wt)-1, respectively). [Cl-]i at 18.3 +/- 0.5 mmol (kg wet wt)-1 increased (P < 0.0008) compared to controls at 15.8 +/- 0.5 mmol (kg wet wt)-1. Thus, in these rats, evidence for an inhibition of the Na+ pump was no longer observed. This points to a major intrinsic mechanism within the kidney for mediating natriuresis, since circulating factors were identical to those in the unsnared kidney, where significant natriuresis occurred.

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