Dynamics and contribution of mechanisms mediating renal blood flow autoregulation.
We investigated dynamic characteristics of renal blood flow (RBF) autoregulation and relative contribution of underlying mechanisms within the autoregulatory pressure range in 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 rapid step reduction and RAP rise. In response to rise, RVR initially fell 5-10% and subsequently increased approximately 20%, reflecting 93% autoregulatory efficiency (AE). Within the initial 7-9 s, RVR rose to 55% of total response providing 37% AE, reaching maximum speed at 2.2 s. A secondary RVR increase began at 7-9 s and reached maximum speed at 10-15 s. Response times suggest that the initial RVR reflects the myogenic response and the secondary tubuloglomerular feedback (TGF). During TGF inhibition by furosemide, AE was 64%. The initial RVR rise was accelerated and enhanced, providing 49% AE, but it represented only 88% of total. The remaining 12% indicates a third regulatory component. The latter contributed up to 50% when the RAP increase began below the autoregulatory range. TGF augmentation by acetazolamide affected neither AE nor relative myogenic contribution. Diltiazem infusion markedly inhibited AE and the primary and secondary RVR increases but left a slow component. In response to RAP reduction, initial vasodilation constituted 73% of total response but was not affected by furosemide. The third component's contribution was 9%. Therefore, RBF autoregulation is primarily due to myogenic response and TGF, contributing 55% and 33-45% in response to RAP rise and 73% and 18-27% to RAP reduction. The data imply interaction between TGF and myogenic response affecting strength and speed of myogenic response during RAP rises. The data suggest a third regulatory system contributing <12% normally but up to 50% at low RAP; its nature awaits further investigation.
Just
Armin
A
Dept. of Cell and Molecular Physiology, 6341 Medical Biomolecular Research Bldg., CB#7545, School of Medicine, Univ. of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7545, USA. just@med.unc.edu
Arendshorst
William J
WJ
D000086:Acetazolamide / Q000494:pharmacology; D000758:Anesthesia; D000818:Animals; D001011:Aorta / Q000502:physiology; D001160:Arterioles / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004110:Diltiazem / Q000494:pharmacology; D004232:Diuretics / Q000494:pharmacology; D025461:Feedback, Physiological / Q000502:physiology; D005665:Furosemide / Q000494:pharmacology; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology*; D007678:Kidney Glomerulus / Q000098:blood supply*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology*
D002121:Calcium Channel Blockers; D004232:Diuretics; D005665:Furosemide; D004110:Diltiazem; D000086:Acetazolamide