1. The diseased kidney in the dog with experimental unilateral reduction in nephron population, has been shown previously to undergo an exaggerated inhibition of sodium reabsorption after extracellular fluid (ECF) volume expansion induced by isotonic sodium chloride solution compared with the control kidney. The latter serves to maintain a non-azotaemic environment.
2. In the present studies, manoeuvres designed to alter predominantly either post-glomerular hydrostatic pressure (PGHP) or peritubular capillary oncotic pressure (COP) were performed to investigate further the mechanism of this exaggerated natriuresis.
3. Volume expansion with 5 g/dl albumin in 145 mmol/l sodium chloride (saline), thereby increasing PGHP without changing COP, produced exaggerated diseased kidney natriuresis, but of a smaller magnitude than when the same dogs were studied under a lesser degree of intravascular volume expansion with 145 mmol/l saline. Renal vasodilatation produced by systemically administered dopamine, which increases PGHP without ECF volume expansion, also produced exaggerated natriuresis by the diseased kidney.
4. A selective decrease in COP induced by expansion with saline in conjunction with trimethophan camsylate (Arfonad)-induced hypotension also produced exaggerated diseased kidney natriuresis, but to a lesser degree than saline expansion alone in the same dogs.
5. Thus experimental manoeuvres designed to reduce peritubular capillary fluid reabsorption by either predominantly increasing PGHP or decreasing COP produced exaggerated diseased kidney natriuresis. This exaggerated natriuretic response to manoeuvres which predominantly altered either physical force by itself did not approach the response elicited by expansion with saline.
6. The data suggest that alterations in Starling forces play an important role in mediating the exaggerated diseased kidney natriuresis after an acute saline load.