Effect of changes in renal perfusion pressure on the suppression of proximal tubular sodium reabsorption due to saline loading.

Rapid intravenous infusion of saline is known to suppress reabsorption of sodium and water in the proximal tubule. It has previously been shown that this suppression is accompanied by two changes which in combination might account for the over-all decrease in reabsorption: a reduction in the intrinsic reabsorptive capacity of the tubular epithelium (C/pir(2)) and a reduction in the ratio between tubular volume and GFR (pir(2)d/V(o)). The present micropuncture experiments were carried out in order to study the possible role of altered peritubular physical forces (hydrostatic and colloid oncotic pressure) in mediating these two changes. Proximal tubular reabsorptive capacity, transit time, fractional reabsorption of sodium and water, pir(2)d/V(o), and intratubular hydrostatic pressure were measured in saline-loaded rats during acute changes in renal perfusion pressure induced by intermittent constriction of the abdominal aorta. We found that when renal perfusion pressure was lowered to 70-90 mm Hg, the usual effects of saline loading on C/pir(2), pir(2)d/V(o), and fractional reabsorption in the proximal tubule were greatly minimized. When the aortic clamp was released and renal perfusion pressure allowed to rise, C/pir(2), pir(2)d/V(o), and fractional reabsorption fell markedly to levels characteristically seen in saline diuresis. Reclamping of the aorta reversed all of these changes. In order to determine whether the changes in C/pir(2) accompanying changes in renal perfusion pressure were mediated by a circulating natriuretic hormone, we assayed in hydopenic rats the dialysate of plasma collected from saline-loaded rats during and after release of aortic constriction by the split oil drop method. No significant difference in reabsorptive half-time (t(1/2)) was found between the two dialysates, and t(1/2) with both dialysates was approximately the same as was found when isotonic saline was injected in the tubules of hydropenic control animals. These observations suggest that the large changes in C/pir(2) which occurred with changes in renal perfusion pressure in saline-loaded rats were not mediated by a circulating hormone. We suggest that the reduction in C/pir(2), pir(2)d/V(o), and fractional reabsorption which occurs in the proximal tubule during a saline diuresis is related to the rise in hydrostatic pressure within the kidney.