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• W1966187721 abstract "<i>Background:</i> In early type 1 diabetes mellitus, changes in proximal reabsorption influence glomerular filtration rate (GFR) through tubuloglomerular feedback (TGF). Due to TGF, a <i>primary</i> increase in proximal reabsorption causes early diabetic hyperfiltration, while a heightened sensitivity of the proximal tubule to dietary salt leads to the so-called salt paradox, where a change in dietary salt causes a reciprocal change in GFR (‘tubulocentric principle’). Here, experiments were performed in adenosine A₁ receptor knockout mice (A₁R–/–), which lack an immediate TGF response, to determine whether A₁Rs are essential for early diabetic hyperfiltration and the salt paradox. <i>Methods:</i> GFR was measured by inulin disappearance in conscious A₁R–/– and wild-type (WT) mice after 4 weeks of streptozotocin diabetes on a control NaCl diet (1%), and measurements were repeated after 6 days of equilibration on a low-NaCl (0.1%) or a high-NaCl (4%) diet. <i>Results:</i> A₁R–/– and WT were similar with respect to blood glucose, dietary intakes and body weight changes on a given diet. Diabetic hyperfiltration occurred in WT, but was blunted in A₁R–/–. A reciprocal relationship between GFR and dietary salt was found in WT diabetics, but not A₁R–/– diabetics or nondiabetics of either strain. <i>Conclusion:</i> A₁Rs determine glomerular hyperfiltration and the salt paradox in early diabetes, which is consistent with the tubulocentric principle." @default.
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• W1966187721 date "2009-03-10" @default.
• W1966187721 modified "2023-10-13" @default.
• W1966187721 title "Adenosine A₁ Receptors Determine Glomerular Hyperfiltration and the Salt Paradox in Early Streptozotocin Diabetes Mellitus" @default.
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• W1966187721 doi "https://doi.org/10.1159/000208211" @default.
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