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���Ѵ���(English) This research has been performed to elucidate theeffect and the mechanism of action of stevioside (SVS)on the renal function in rats. An intravenous infusionof SVS (150 mg/ml) in the small, medium and large doses(100,150,200 mg/kg.BW) reduced blood pressure to thelowest values in the dose-dependent manner within 5-7min.(P<0.001). Blood pressure gradually increasedafterward but not to the normal level while heart ratecontinuously increased in rats treated with the largeand medium doses of SVS infusion. The initial decreaseof blood pressure could be reversed after pretreatedwith L-NAME whereas both hypotension and techycardia inthe latter period was reversed by pretreatment withindomethacin. Animals pretreated with prazosin reducedblood pressure and heart rate (P<0.001) both before andduring SVS infusion while pretreatment withnorepinephrine showed the opposite results. The plasmavolume and blood volume were not significantly affectedduring SVS infusion. SVS intubation (2 g/kg.BW) for 6hours also induced hypotension but with a slightextent. The first 30-min of SVS infusion raisedERBF(P<0.05)without a change of GFR. ERBF was unalteredafterward while GFR reduced (P<0.05) after cessation ofSVS infusion in animals treated with the large andmedium doses. SVS feeding had no effect on renalhemodynamics. Renal vasodilatation action by SVSinfusion could be reversed in rats pretreated withindomethacin or arginine vasopressin (AVP). Thecogestion of glomerular capillaries fromhistopathological examination was noted in animalstreated with the large and medium doses. The fractional excretion of Na('+)(FE(,Na),Cl('-) (FE(,Cl)),glucose (FE(,G)) andK('+)(FE(,K)) was significantly raised in both duringand after SVS infusion. The lithium clearance methodshowed that the depression of proximal tubular Na('+)and water reabsorption correlated to the elevation ofFE(,Na). The first 30-min of SVS infusion suppressedthe renal mitochondrial activity and Na('+),K('+)ATPaseactivity (P<0.05) approximately 14% and 21%respectively while proximal tubular reabsorption ofNa('+) reduced 88%. The rise of FE(,Na) and FE(,Cl)remained no matter how a change of renal hemodynamicswas occured or not. Pretreatment with indomethacin orAVP reversed the rise of electrolyte excretion duringthe second period of SVS infusion. SVS intubation alsoincreased electrolyte excretion (P<0.05) without achange of FE(,G). SVS infusion raised the plasmaglucose level (P(,G)(P<0.001)) but P(,G) was stilllower than the renal plasma threshold of glucose innormal rats (264(+,-)19.25 mg%). Moreover renal tubularreabsorption of glucose during SVS infusion was lowerthan the tubular transport maximum of glucose (Tm(,G)).SVS infusion raised P(,G) by decrease in glucose uptakewithout a change in insulin release. Hyperglycemiceffect of SVS infusion was attenuated afterpretreatment with L-NAME or prazosin or indomethacin,but returned to normal after pretreatment with acombination of L-NAME and indomethacin. It can beconcluded that the hypotension and tachycardia weremediated via NO, prostaglandin and sympathetic activityduring SVS infusion. SVS infusion caused a dilation ofboth afferent and efferent arterioles. An increase inelectrolyte and glucose excretion induced by SVSinfusion was the reduction of proximal tubularreabsorption of Na('+) whereas SVS intubation exertedits effect on distal part of nephron. The hyperglycemiceffect by the action of SVS infusion was theinteraction among NO, prostaglandin and sympatheticactivity. SVS infusion also inhibitedglucose-stimulated insulin release.