Background: 

Evidence supports involvement of adenosine and ATP in renal blood flow (RBF) autoregulation, but controversy exists regarding the role of ATP in tubuloglomerular feedback (TGF). Since RBF autoregulation is caused by the myogenic response (MR), TGF, and a third, unidentified, regulatory mechanism, we tested the hypothesis that ATP does not mediate TGF, but the third mechanism.

Methods: 

RBF autoregulation and the three regulatory mechanisms were assessed from the response of RBF to rapid experimental changes in renal artery pressure (RAP) in anesthetized rats. The response within the first 6 s after the RAP-rise was interpreted as MR, that between 6 and 25 s as TGF, and 25 to 100 s as third mechanism. A1 adenosine receptors (A1AR) were inhibited by DPCPX (600 mg/kg iv.), and P2X1 ATP receptors (P2X1R) by Suramin (10 mg/kg/min ia.).

Results: 

Suramin abolished P2X1R-responses, but did not affect (p>0.09) total autoregulation (94±6 vs. 96±6% of perfect), MR (34±4 vs. 42±6 regulatory units), TGF (29±4 vs. 35±3 units), or the third mechanism (51±7 vs. 37±2 units). In contrast, DPCPX diminished total autoregulation (72±8 vs. 99±6%, p<0.05) and virtually abolished TGF (9±6 vs. 39±4 units, p<0.001), without affecting (p>0.5) MR (57±7 vs. 60±5 units) or third mechanism (15±4 vs. 21±6 units).

Conclusions: 

P2X1R do not contribute to RBF autoregulation, TGF, or the third autoregulatory mechanism. A1AR, by contrast, support RBF autoregulation by mediating TGF.