Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury
R Faulhaber-Walter, L Chen… - Journal of the …, 2008 - journals.lww.com
Intraglomerular hypertension and glomerular hyperfiltration likely contribute to the
pathogenesis of diabetic nephropathy, and tubuloglomerular feedback (TGF) has been
suggested to play a role in diabetic hyperfiltration. A1 adenosine receptor (A1AR) null mice
lack a TGF response, so this model was used to investigate the contribution of TGF to
hyperfiltration in diabetic Ins2+/− Akita mice. TGF responses in Ins2+/− A1AR−/− double
mutants were abolished, whereas they were attenuated in Ins2+/− mice. GFR, assessed at …
pathogenesis of diabetic nephropathy, and tubuloglomerular feedback (TGF) has been
suggested to play a role in diabetic hyperfiltration. A1 adenosine receptor (A1AR) null mice
lack a TGF response, so this model was used to investigate the contribution of TGF to
hyperfiltration in diabetic Ins2+/− Akita mice. TGF responses in Ins2+/− A1AR−/− double
mutants were abolished, whereas they were attenuated in Ins2+/− mice. GFR, assessed at …