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1 Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
* To whom correspondence should be addressed. E-mail: just{at}med.unc.edu.
We investigated dynamic characteristics of renal blood flow (RBF) autoregulation and the relative contribution of the underlying mechanisms within the autoregulatory pressure range in Sprague-Dawley rats. Renal arterial pressure (RAP) was reduced by suprarenal aortic constriction for 60 s, and then rapidly released. Changes in renal vascular resistance (RVR) were assessed following the rapid step reduction and rise in RAP. In response to the rise, RVR initially fell 5-10% and subsequently increased ~20%, reflecting autoregulatory efficiency (AE) of 93%. Within the initial 7-9 s, RVR rose to 55% of the total response providing AE of 37%, reaching maximum speed at 2.2 s. A secondary RVR increase began at 7-9 s and reached maximum speed at 10-15 s. The response times suggest that the initial RVR reflects the myogenic response and the secondary tubuloglomerular feedback (TGF). During inhibition of TGF by furosemide, AE was 64%. The initial rise in RVR was accelerated (0.29 vs 0.20 mmHg/(ml/min/g)/s, p<0.05) and enhanced, providing AE of 49% (p=0.005 vs 37%), but it represented only 88% of the total response. The remaining 12% indicates participation of a third regulatory component. The latter contributed up to 50% when the step increase in RAP began below the autoregulatory range. Augmentation of TGF by acetazolamide affected neither AE nor the relative myogenic contribution. Infusion of the Ca2+-channel blocker diltiazem markedly inhibited AE and the primary and secondary increases of RVR but left a slow component. In response to reduction of RAP the initial vasodilation constituted 73% of the total response, but was not affected by furosemide. Contribution of the third component was 9%. In conclusion, RBF autoregulation is primarily due to myogenic response and TGF, contributing 55% and 33-45% in response to a rise and 73% and 18-27% to reduction of RAP. The data imply interaction between TGF and myogenic response affecting strength and speed of the myogenic response during rises of RAP. The data suggest a third regulatory system contributing <12% normally, but up to 50% at low RAP; its nature awaits further investigation.
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