V. Vallon et al., EFFECT OF CHRONIC SALT LOADING ON KIDNEY-FUNCTION IN EARLY AND ESTABLISHED DIABETES-MELLITUS IN RATS, The Journal of laboratory and clinical medicine, 130(1), 1997, pp. 76-82
Glomerular hyperfiltration and renal hypertrophy are among the events
that characterize the early course of diabetes mellitus in rats and hu
man patients. Previous studies from this laboratory demonstrated that
salt restriction paradoxically reduces total renal vascular resistance
(RVR) and increases glomerular filtration rate (GFR) in diabetic rats
(J Am Soc Nephrol 2995;5:1751-7), In the present study we examined th
e converse condition by testing the effects of chronic salt loading on
kidney function in moderately hyperglycemic insulin-treated rats with
early and established streptozotocin diabetes. Salt loading was accom
plished by adding 1% NaCl to the drinking water 1 day or 35 days after
diabetes was induced. The high-salt diet appropriately increased salt
excretion in diabetic rats and nondiabetic controls. GFR and renal pl
asma flow were determined by inulin and para-amino hippuric acid (PAH)
clearance 7 days after salt loading was started. Diabetic rats receiv
ing tap water exhibited hyperfiltration with no change In renal blood
flow (RBF). In nondiabetic rats, salt loading caused a reduction in to
tal RVR and proportional increases in RBF, GFR, and kidney weight (KW)
. Salt loading in early diabetes did not affect RVR, RBF, or KW and ca
used a paradoxical reduction in GFR. In established diabetes, salt loa
ding reduced RVR and increased RBF, similar to results in nondiabetic
rats, but as in rats with early diabetes, if did not Increase GFR or K
W. In summary, although the response in RVR and RBF to chronic salt lo
ading depends on the duration of diabetes, the increase in GFR and KW
as seen in nondiabetic rats is blunted in the early and established st
ate of insulin-treated diabetes in rats, These findings further suppor
t the notion that the renal response to variation in salt intake is al
tered in insulin-treated diabetes In rats.