ArticleAmerican journal of physiology. Renal physiology2013
Angiotensin II contributes to glomerular hyperfiltration in diabetic rats independently of adenosine type I receptors.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 30 citations in OpenAlex.
- Molecular Mechanisms and Clinical Evidence Supporting the Four Pillars of Therapy in Diabetic Kidney Disease: Emerging Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Estimated Glomerular Filtration Rate and Incident Prediabetes Risk in Normoglycemic Adults With Parental Type 2 Diabetes.Journal of the Endocrine Society · 2025Article
- Article
- Elucidating the function of clusterin in the progression of diabetic kidney disease.Frontiers in pharmacology · 2025Review
- Renal handling of albumin in rats with early stage diabetes: A theoretical analysis.The Journal of physiology · 2024Article
- Molecular pathways that drive diabetic kidney disease.The Journal of clinical investigation · 2023Review
- Blocking angiotensin 2 receptor attenuates diabetic nephropathy via mitigating ANGPTL2/TL4/NF-κB expression.Molecular biology reports · 2021Article
- Adenosine ABiomedicines · 2020Article
- Diabetes downregulates renal adenosine A2A receptors in an experimental model of hypertension.PloS one · 2019Article
- Endothelin type A receptor inhibition normalises intrarenal hypoxia in rats used as a model of type 1 diabetes by improving oxygen delivery.Diabetologia · 2015Article
- Glucose Homeostasis and Cardiovascular Alterations in Diabetes.Comprehensive Physiology · 2015Review
- Recent advances in renal hemodynamics: insights from bench experiments and computer simulations.American journal of physiology. Renal physiology · 2015Review
- Blood pressure, heart rate and tubuloglomerular feedback in A1AR-deficient mice with different genetic backgrounds.Acta physiologica (Oxford, England) · 2015Article
- Proteomics and diabetic nephropathy: what have we learned from a decade of clinical proteomics studies?Journal of nephrology · 2014Review
- Arrestin(g) podocyte injury with endothelin antagonism.Journal of the American Society of Nephrology : JASN · 2014Article
- Activation of adenosine receptors improves renal antioxidant status in diabetic Wistar but not SHR rats.Upsala journal of medical sciences · 2014Article
- Intrarenal renin-angiotensin system in regulation of glomerular function.Current opinion in nephrology and hypertension · 2014Review
- Endothelin receptor a blockade is an ineffective treatment for adriamycin nephropathy.PloS one · 2013Article
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6 authors at 3 institutions in 2 countries.
Funding
Abstract
Increased angiotensin II (ANG II) or adenosine can potentiate each other in the regulation of renal hemodynamics and tubular function. Diabetes is characterized by hyperfiltration, yet the roles of ANG II and adenosine receptors for controlling baseline renal blood flow (RBF) or tubular Na(+) handling in diabetes is presently unknown. Accordingly, the changes in their functions were investigated in control and 2-wk streptozotocin-diabetic rats after intrarenal infusion of the ANG II AT1 receptor antagonist candesartan, the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), or their combination. Compared with controls, the baseline blood pressure, RBF, and renal vascular resistance (RVR) were similar in diabetics, whereas the glomerular filtration rate (GFR) and filtration fraction (FF) were increased. Candesartan, DPCPX, or the combination increased RBF and decreased RVR similarly in all groups. In controls, the GFR was increased by DPCPX, but in diabetics, it was decreased by candesartan. The FF was decreased by candesartan and DPCPX, independently. DPCPX caused the most pronounced increase in fractional Na(+) excretion in both controls and diabetics, whereas candesartan or the combination only affected fractional Li(+) excretion in diabetics. These results suggest that RBF, via a unifying mechanism, and tubular function are under strict tonic control of both ANG II and adenosine in both control and diabetic kidneys. Furthermore, increased vascular AT1 receptor activity is a contribution to diabetes-induced hyperfiltration independent of any effect of adenosine A1 receptors.
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