SummaryThe renal excretion of water, sodium, and potassium was measured together with glomerular filtration rate (mannitol clearance) and effective renal plasmal flow (sodium p-amino-hippurate clearance) before, during, and after elevation of abdominal pressure by the application of a pneumatic girdle inflated at 80 mm Hg. The response observed, in 6“normal”subjects (5 without evidence of cardiovascular or renal disease and I with uncomplicated hypertensive vascular disease) did not differ appreciably from that in 5 subjects with well-established diabetes insipidus.Glomerular filtration and renal plasma flow decreased during compression, as noted in previous studies. Sodium excretion and urine flow fell more than filtration whereas the output of potassium diminished to the same extent. The urinary sodium concentration nearly always decreased suggesting that urine flow fell secondarily as a result of an active increase in tubular reabsorption of sodium (presumably in the proximal segment). The available evidence indicates that filtration falls because a fraction of the nephron population ceases to function and that perfusion and filtration in the active nephrons remain unchanged, apparently eliminating these alterations as possible causative factors.It was suggested that the elevation in renal venous pressure coupled with the obstructive rise in renal pelvic pressure played a primary role in augmenting proximal tubular reabsorption of sodium with a secondary passive increase in reabsorption of water.