[The mechanism of renal hyperperfusion induced by hyperglycemia].
Using whole body clearance technique as well as isolated perfused rat kidney (IPRK). We studied the effect of hyperglycemia on renal hemodynamics and the possible mechanism involved. Hyperglycemia increased renal plasma flow (RPF) and glomerular filtration rate (GFR). In nonfiltering isolated perfused rat kidney or after adding furosemide to the perfusate, both techniques were believed to abolish the tubuloglomerular feedback, the renal hemodynamic changes induced by hyperglycemia disappeared, but adding sodium nitroprusside increased RPF and decreased renal vascular resistance (RVR). D-alpha-methyl-glucoside, a glucose derivative, increased RPF and GFR in IPRK, but had no influence on renal hemodynamics in whole body clearance study. Hemoglobin, which could block the action of endothelium--derived relaxing factor (EDRF), did not change the effects of hyperglycemia on renal hemodynamics in IPRK. These results indicated that hyperglycemia could directly induce hyperperfusion and hyperfiltration, which is mainly mediated by suppression of tubuloglomerular feedback. EDRF do not play the major role in the changes of hemodynamics induced by hyperglycemia.
Qi
Z H
ZH
Nephrology Research Laboratory, Hua Shan Hospital, Shanghai Medical University.
Li
S Y
SY
Hao
C M
CM
D000818:Animals; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006439:Hemodynamics; D006943:Hyperglycemia / Q000503:physiopathology*; D066298:In Vitro Techniques; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D008757:Methylglucosides / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D017595:Renal Plasma Flow / Q000187:drug effects; D014655:Vascular Resistance
D008757:Methylglucosides; D009569:Nitric Oxide; C027020:methylglucoside