title: Increased susceptibility to hypertensive renal disease in streptozotocin-treated diabetic rats is not modulated by salt intake.
abstract: OBJECTIVE
  In early type 1 diabetes mellitus, renal salt handling is dysregulated, so that the glomerular filtration rate becomes inversely proportional to salt intake. The salt paradox occurs in both humans and rats and, with low salt intake, results in diabetic hyperfiltration. We tested whether increased salt intake could reduce the susceptibility to injury of non-clipped kidneys in diabetic rats with pre-existing Goldblatt hypertension.
  
  
  METHODS
  Male Long-Evans rats were made hypertensive and half were then made diabetic. Blood glucose was maintained at ~20-25 mmol/l by insulin implants. One half of each received only the salt in normal chow (1% by weight) and the other half received added salt in drinking water to equal 2.7% by weight of food intake. Weekly 24 h blood pressure records were acquired by telemetry during the 4-month experiment.
  
  
  RESULTS
  Systolic blood pressure was not affected by diabetes or increased salt intake, alone or together. Autoregulation was highly efficient in the non-clipped kidney of both intact and diabetic rats. Histological examination showed minor injury in the clipped kidney, which did not differ among groups. The non-clipped kidney showed extensive pressure-dependent glomerular and vascular injury in both intact and diabetic rats.
  
  
  CONCLUSIONS
  The relationship between pressure and injury was shifted toward lower blood pressure in diabetic rats, indicating that diabetes increased the susceptibility of the kidney to injury despite preservation of autoregulation. The increased susceptibility was not affected by high salt intake in the diabetic rats, thus disproving the hypothesis.
authors.affiliation: Department of Biology, University of Victoria, Victoria, BC, Canada.
authors.forename: C A
authors.initials: CA
authors.lastname: Sima
authors.forename: M P
authors.initials: MP
authors.lastname: Koeners
authors.forename: J A
authors.initials: JA
authors.lastname: Joles
authors.forename: B
authors.initials: B
authors.lastname: Braam
authors.forename: A B
authors.initials: AB
authors.lastname: Magil
authors.forename: W A
authors.initials: WA
authors.lastname: Cupples
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000503:physiopathology; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism* / Q000503:physiopathology; D003928:Diabetic Nephropathies / Q000378:metabolism* / Q000503:physiopathology; D004198:Disease Susceptibility; D006973:Hypertension / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D051381:Rats; D020318:Rats, Long-Evans; D012079:Renal Circulation; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage / Q000494:pharmacology*; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D017673:Sodium Chloride, Dietary