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Reduced autoregulatory effectiveness in adenosine 1 receptor-deficient mice

National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland

Submitted 22 September 2005 ; accepted in final form 27 October 2005

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 tubuloglomerular feedback (TGF) mechanisms. Using mice with deletion of the A₁ adenosine receptor (A1AR) gene, we 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) were 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 mmHg in A1AR–/– (n = 9) and by 14.2 ± 0.9 mmHg 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 = 0.013). Similarly, with pressure reductions of 14.8 ± 1.1 and 13.3 ± 1.5 mmHg in A1AR–/– (n = 9) and wild-type mice (n = 8), respectively (P = 0.43), RBF fell by 0.17 ± 0.02 ml/min in A1AR–/– mice and by only 0.08 ± 0.02 ml/min in wild-type animals (P = 0.0039). Autoregulatory indexes for both GFR and RBF were significantly higher in A1AR–/– compared with 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.

glomerular filtration rate; renal blood flow; aortic clamp; autoregulatory index

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