Responsiveness of renal glomeruli to adenosine in streptozotocin-induced diabetic rats dependent on hyperglycaemia level

Glomerular filtration rate (GFR) in response to adenosine precursor, NAD, and glomeruli contractility in response to adenosine were evaluated in streptozotocin-induced diabetic rats with severe (blood glucose 27.8 +/- 1.2 mmol/L) and moderate hyperglycaemia (18.2 +/- 0.9 mmol/L) compared with nondia...

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Published in:Journal of physiology and pharmacology : an official journal of the Polish Physiological Society 2003-03, Vol.54 (1), p.109-120
Main Authors: Szczepańska-Konkel, M, Jankowski, M, Stiepanow-Trzeciak, A, Rudzik, A, Pawełczyk, T, Angielski, S
Format: Article
Language:English
Subjects:
Adenosine - physiology
Animals
Blood Glucose - physiology
Diabetes Mellitus, Experimental - physiopathology
Glomerular Filtration Rate - drug effects
Hemodynamics - drug effects
Hemodynamics - physiology
Inulin
Kidney Glomerulus - drug effects
Kidney Glomerulus - physiopathology
Male
NAD - pharmacology
Purinergic P1 Receptor Antagonists
Rats
Rats, Wistar
Renal Plasma Flow - drug effects
Xanthines - pharmacology
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Summary:Glomerular filtration rate (GFR) in response to adenosine precursor, NAD, and glomeruli contractility in response to adenosine were evaluated in streptozotocin-induced diabetic rats with severe (blood glucose 27.8 +/- 1.2 mmol/L) and moderate hyperglycaemia (18.2 +/- 0.9 mmol/L) compared with nondiabetic (ND)-rats. In anaesthetised rats, basal GFR was greater in moderately diabetic rats compared with severely diabetic rats (p < 0.05) and ND-rats (p < 0.02). Intravenous infusion of 5 nmol x min(-1) x kg(-1) NAD reduced GFR and renal plasma flow (RPF) in diabetic rats but had no effect on these parameters in ND-rats. Moreover, NAD-induced reduction of GFR and RPF was greater in rats with severe diabetes (41% and 30%, respectively) than in with moderate diabetes (25% and 26%, respectively). Theophylline (0.2 micromol x min(-1) x kg(-1) ) abolished renal response to NAD. Isolated glomeruli contraction in response to adenosine, assessed by glomerular 3H-inulin space reduction, was lowered in moderately diabetic-group and enhanced in severely diabetic-group. compared with ND-group (p < 0.05). Adenosine A1-receptor antagonist DPCPX inhibited adenosine-induced glomeruli contraction. This differential response of diabetic renal glomeruli to adenosine suggests that impaired glomerular contractility in response to adenosine could be responsible for hyperfiltration in moderate diabets, whereas, the increased adenosine-dependent contractility of glomeruli in severe diabetes may increase the risk of acute renal failure in this condition.
ISSN:0867-5910