Renal arterial reactivity to potassium, noradrenaline, and neuropeptide Y and association with urinary albumin excretion in the diabetic rat

Abstract

A changed vasomotor reactivity of renal arteries may lead to defect autoregulation of renal hemodynamics with damage of diabetic kidneys. Eleven streptozotocin-induced diabetic male Wistar rats were daily treated with insulin in order to achieve a blood glucose of 21 mmol/L. Seventeen age and gender-matched rats served as controls. After 50 days, the kidneys were rapidly removed, arteria renalis and the first branches of the intrarenal arteries were dissected free. The arterial reactivity was tested with a sensitive in vitro method. The reactivity to noradrenaline was tested by cumulative application (10(-9) to 3 x 10(-4) M) before and after a single concentration of neuropeptide Y (NPY). Potassium (60 mM) and noradrenaline induced a strong contraction of all arteries with similar response in diabetic and control rats. The effect of noradrenaline after NPY was unchanged in renal vessels of control rats, whereas it was diminished in intrarenal vessels for both diabetic and control rats. Similarly, a diminished response was found for renal arteries in diabetic rats, an effect which was related to the level of blood glucose (r = 0.62, 2p = 0.04). The urinary excretion rate of albumin in the diabetic rats was related to the largest noradrenaline induced contraction (r = 0.71, 2p = 0.01) of renal but not of intrarenal arteries. In conclusion, there was no difference in potassium and noradrenaline evoked contractions in renal and intrarenal arteries in diabetic and control rats. NPY decreased the contractile response to noradrenaline. The high blood glucose slightly increased this effect of NPY.