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

The characteristics of the tubuloglomerular feedback (TGF) mechanism were examined in streptozotocin-diabetic rats. This model is known to induce damage in the distal tubular system and thus Tamm-Horsfall protein (THP) secretion. Three groups of male Sprague-Dawley rats were studied: (A) diabetic rats 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 normal. This indicates that the diabetic animals of this study were severely vasoconstricted. 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. The 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 pressure and an increased TGF reactivity, which indicates that the diabetic rats were vasoconstricted. NOS inhibition increased the reactivity of TGF to greater extent in diabetic animals than in controls, indicating that the renal vasoconstriction was compensated for by an increased NO production. (C) 2000 Elsevier Science Inc. All rights reserved.