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1 National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
* To whom correspondence should be addressed. E-mail: jurgens{at}intra.niddk.nih.gov.
Adjustments of renal vascular resistance in response to changes in blood pressure are mediated by an interplay between the myocyte-inherent myogenic and the kidney-specific TGF mechanisms. Using mice with deletion of the A1 adenosine receptor (A1AR) gene we have tested the prediction that the absence of TGF, previously established to result from A1AR deficiency, is associated with a reduction in the efficiency of autoregulation. In anesthetized wild type (A1AR+/+) and A1AR-deficient mice (A1AR-/-) glomerular filtration rate (GFR) and renal blood flow (RBF) was determined before and after reducing renal perfusion pressure through a suprarenal aortic clamp. In response to a blood pressure reduction by 15.9 ± 1.34 mm Hg in A1AR-/- (n=9) and by 14.2 ± 0.9 mm Hg in A1AR+/+ mice (n=8; p=0.31), GFR fell by 187.9 ± 37 µl/min and by 72.3 ± 10 µl/min in A1AR-/- and A1AR+/+ mice respectively (p=.013). Similarly, with pressure reductions of 14.8 ± 1.1 and 13.3 ± 1.5 mm Hg in A1AR-/- (n=9) and wild type mice (n=8) respectively (p=0.43), RBF fell by 0.17 ± .02 ml/min in A1AR-/- mice and by only 0.08 ± .02 ml/min in wild type animals (p=0.0039). Autoregulatory indeces for both GFR and RBF were significantly higher in A1AR-/- compared to A1AR+/+ mice indicating reduced regulatory responsiveness in the knockout animals. We conclude that autoregulation of renal vascular resistance is less complete in A1AR-deficient mice, an effect that is presumably related to absence of TGF regulation in these animals.
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