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Deep intrarenal venous pressure was used as an index of renal capillary pressure to test the proposal that physically induced changes in sodium reabsorption may be mediated by changes in Starling forces across the capillary. Renal vasodilatation produced natriuresis associated with immediate increases in intrarenal venous pressure. Increased arterial pressure was accompanied by further natriuresis and initially increased intrarenal pressure in vasodilated kidneys. Plasma load was always accompanied by increased intrarenal venous pressure. Saline loading usually increased intrarenal venous pressure, and restoration of plasma protein concentration during saline loading reduced, but did not abolish, natriuresis. This continued natriuresis was associated with reduced renal vascular resistance and increased intrarenal venous pressure, demonstrating that continued natriuresis after restoring plasma oncotic pressure during saline loading could relate to increased capillary hydrostatic pressure. Intrarenal venous pressure did not relate to isolated changes in urine flow, arterial pressure, or renal blood flow. These observations support the hypothesis that changes in peritubular capillary hydrostatic pressure initiate changes in tubular sodium reabsorption as a result of changes in capillary uptake.

Relationship between Intrarenal Hydrostatic Pressure and Hemodynamically Induced Changes in Sodium Excretion