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Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats.
Fructose-induced metabolic syndrome is associated with renal disturbances characterized by renal hypertrophy, arteriolopathy, glomerular hypertension, and cortical vasoconstriction, best observed in rats administered high doses (60% diet) of fructose. Expand
Renal angiotensin II concentration and interstitial infiltration of immune cells are correlated with blood pressure levels in salt-sensitive hypertension.
Blood pressure correlated positively with interstitial AII and negatively with plasma AII, thus giving compelling evidence of the paramount role of the AII within the kidney in the A II-induced model of salt-driven hypertension. Expand
Mild hyperuricemia induces glomerular hypertension in normal rats.
Mildly hyperuricemic rats develop renin-dependent hypertension and interstitial renal disease. Hyperuricemia might also induce changes in glomerular hemodynamics. Micropuncture experiments under deepExpand
Effects of febuxostat on metabolic and renal alterations in rats with fructose-induced metabolic syndrome.
Normalization of plasma UA with Fx in rats with metabolic syndrome alleviated both metabolic and glomerular hemodynamic and morphological alterations, providing further evidence for a pathogenic role of hyperuricemia in fructose-mediated metabolic syndrome. Expand
Treatment with the xanthine oxidase inhibitor febuxostat lowers uric acid and alleviates systemic and glomerular hypertension in experimental hyperuricaemia.
Febuxostat (Fx), an investigational, nonpurine and selective xanthine oxidase inhibitor, is a more effective UA-lowering agent than allopurinol in OA-induced hyperuricaemic rats and merits further evaluation for the treatment of hypertension and renal alterations induced byhyperuricaemia. Expand
Effect of Febuxostat on the Progression of Renal Disease in 5/6 Nephrectomy Rats with and without Hyperuricemia
Fx prevented renal injury in 5/6 Nx rats with and without coexisting hyperuricemia, and helped to preserve preglomerular vessel morphology, normal glomerular pressure was maintained even in the presence of systemic hypertension. Expand
Effect of adenosine A1 analogue on tubuloglomerular feedback mechanism.
It is demonstrated that intraluminal administration of anadenosine A1 analogue causes feedback-mediated decreases in SFP and therefore support a role for adenosine receptors in the signal transmission pathway. Expand
Hypothyroidism attenuates protein tyrosine nitration, oxidative stress and renal damage induced by ischemia and reperfusion: effect unrelated to antioxidant enzymes activities
Hypothyroidism was able to prevent not only oxidative but also nitrosative stress induced by IR, and the antioxidant enzymes catalase, glutathione peroxidase, and superoxide dismutase seem not to play a protective role in this experimental model. Expand
Effect of phlorizin on SGLT2 expression in the kidney of diabetic rats.
SGLT2 inhibition prevented the development of hypertension in diabetic rats as well as hyperglycemia, suggesting a hypertensive mechanism associated with S GLT2 activity and the likelihood that increased SGLT 2 expression may be associated with progression of diabetic renal complications. Expand
Role of oxidative stress in the renal abnormalities induced by experimental hyperuricemia.
The hypothesis that oxidative stress might contribute to the endothelial dysfunction and glomerular hemodynamic changes that occur with hyperuricemia was tested and scavenging of the superoxide anion in this setting attenuates the adverse effects induced by hyperURicemia. Expand