Renal medullary plasma flow rate and reabsorption of salt and water from inner medullary collecting duct.

It has been proposed that medullary washout secondary to increased blood flow will limit maximal urine osmolality and reabsorption of salt and water from the inner medullary collecting duct. We have tested this prediction. The function of the inner medullary collecting duct was examined by microcatheterization. Acetylcholine was infused directly into the renal circulation, captopril was infused intravenously, and angiotensin II was infused into the renal circulation in rats which also received captopril. Medullary plasma flow rate, measured by dye-dilution in parallel experiments, was not significantly increased by acetylcholine; it was increased 30% (p less than 0.02) by systemic infusion of captopril, and was returned to control by angiotensin II. Acetylcholine increased both urine flow rate and sodium excretion (p less than 0.01, p less than 0.001, respectively), while captopril increased only sodium excretion (p less than 0.025). Angiotensin II blocked the natriuresis due to captopril. None of the treatments altered urine osmolality (p greater than 0.4 in all cases). Acetylcholine increased the loads of water, sodium, chloride, and total solute delivered to the inner medullary collecting duct. Angiotensin II reduced delivery of water and solutes compared with captopril alone. None of the treatments affected load dependency of reabsorption of water, sodium, chloride, or total solute in the inner medullary collecting duct. We conclude that there is, at most, a weak interaction between medullary blood flow and reabsorption from the inner medullary collecting duct.