title: Interactions contributing to kidney blood flow autoregulation.
abstract: OBJECTIVE
  Autoregulation of renal blood flow has traditionally been considered to stabilize glomerular filtration, and thus tubular load, in the face of blood pressure fluctuations. This view arose because of the contribution of tubuloglomerular feedback, which senses distal tubular fluid composition, to regulation and autoregulation of renal blood flow. Studies have indicated a more important role for the myogenic mechanism. It has been proposed that the 'purpose' of autoregulation is to defend glomerular structure. Both these views may be incomplete because neither takes into consideration the complex interactions between tubuloglomerular feedback and the myogenic mechanism and among nephrons whose afferent arterioles derived from a common interlobular artery.
  
  
  RESULTS
  Recent findings indicate that it is now indisputable that effective autoregulation is necessary for defense of glomerular structure. Extensive modulation of the myogenic mechanism by tubuloglomerular feedback has been shown using a variety of experimental designs that have illuminated one pathway (neuronal nitric oxide synthase at the macula densa) by which this occurs.
  
  
  CONCLUSIONS
  These findings indicate that the myogenic mechanism can no longer be considered as a purely vascular mechanism in the kidney and instead receives information via tubuloglomerular feedback about the status of renal function.
authors.affiliation: Centre for Biomedical Research, Department of Biology, University of Victoria, Victoria, British Columbia, Canada. wcupples@uvic.ca
authors.forename: William A
authors.initials: WA
authors.lastname: Cupples
mesh_terms: D000818:Animals; D006706:Homeostasis; D007668:Kidney / Q000098:blood supply* / Q000502:physiology; D007678:Kidney Glomerulus / Q000098:blood supply / Q000502:physiology; D007684:Kidney Tubules / Q000098:blood supply / Q000502:physiology; D008954:Models, Biological; D051381:Rats; D012079:Renal Circulation / Q000502:physiology*; D015398:Signal Transduction