Increased tubuloglomerular feedback reactivity is associated with increased NO production in the streptozotocin-diabetic rat

The characteristics of the tubuloglomerular feedback (TGF) mechanism were e xamined in streptozotocin-diabetic rats. This model is known to induce dama ge in the distal tubular system and thus Tamm-Horsfall protein (THP) secret ion. Three groups of male Sprague-Dawley rats were studied: (A) diabetic ra ts with blood glucose levels (BG) < 19 mmol/l, (B) with BG greater than or equal to 19 mmol/l, and (C) control rats. After 50 days, the diabetic rats had higher arterial blood pressure and increased TGF reactivity (Delta P-SF ) than control rats. The proximal tubular free-flow pressure (P-T) and stop -flow pressure (PSF) were reduced, while the glomerular filtration was norm al. This indicates that the diabetic animals of this study were severely va soconstricted. Inhibition of renal nitric oxide synthase (NOS) resulted in a greater increase of TGF reactivity in diabetic rats than in control rats. Diabetic rats also showed increased excretion rates of albumin and TUP. Th e excretion rate of THP was associated with P-SF (r = -0.88, p < 0.01). In conclusion, diabetes mellitus was associated with an increased blood pressu re and an increased TGF reactivity, which indicates that the diabetic rats were vasoconstricted. NOS inhibition increased the reactivity of TGF to gre ater extent in diabetic animals than in controls, indicating that the renal vasoconstriction was compensated for by an increased NO production. (C) 20 00 Elsevier Science Inc. All rights reserved.