Hyperfiltration occurs in early type 1 diabetes mellitus in both rats and humans. It results from afferent vasodilatation and thus may impair stabilization of glomerular capillary pressure by autoregulation. It is inversely related to dietary salt intake - the "salt paradox". Restoration of normal GFR involves increased pre-glomerular resistance, probably mediated by tubuloglomerular feedback (TGF). To begin to test whether the salt paradox has pathogenic significance, we compared intact versus diabetic (streptozotocin) Long Evans rats with normal and increased salt intake, 1 and ~3% by weight of food eaten, respectively. Weekly 24 h blood pressure records were acquired by telemetry before and during diabetes. Blood glucose was maintained at ~20 mmol/L by insulin implants. GFR was significantly elevated only in diabetic rats on normal salt intake confirming diabetic hyperfiltration and the salt paradox. Renal blood flow dynamics show strong contributions to autoregulation by both TGF and the myogenic mechanism and were not impaired by diabetes or by increased salt intake. Separately, systolic pressure was not elevated in diabetic rats at any time during 12 weeks with normal or high salt intake. Autoregulation was effective in all groups and the diabetic-normal salt group showed significantly improved autoregulation at low perfusion pressures. Histological examination revealed very minor glomerulosclerosis and modest mesangial expansion, although neither was diagnostic of diabetes. Periodic acid-Schiff positive droplets found in distal tubules and collecting duct segments were diagnostic of diabetic kidneys. Biologically significant effects attributable to increased salt intake were abrogation of hyperfiltration and of the left shift in autoregulation in diabetic rats.