renal autoregulation
Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms
Rodger Loutzenhiser,1 Karen Griffin,2
Geoffrey Williamson,3 and Anil Bidani2
1Smooth Muscle Research Group, University of
Calgary, Alberta, Canada; 2Department of
Internal Medicine, Loyola University Medical
Center and Edward Hines, Jr. Veterans Affairs
Hospital, Maywood, Illinois; and 3Department of
Electrical and Computer Engineering, Illinois
Institute of Technology, Chicago, Illinois
ABSTRACT
When the kidney is subjected to acute increases in blood pressure (BP), renal blood flow (RBF) and glomerular filtration rate (GFR) are observed to remain relatively constant. Two mechanisms, tubuloglomerular feedback (TGF) and the myogenic response, are thought to act in concert to achieve a precise moment-by-moment regulation of GFR and distal salt delivery. The current view is that this mechanism insulates renal excretory function from fluctuations in BP. Indeed, the concept that renal autoregulation is necessary for normal renal function and volume homeostasis has long been a cornerstone of renal physiology.
This article presents a very different view, at least regarding the myogenic component of this response. We suggest that its primary purpose is to protect the kidney against the damaging effects of hypertension. The arguments advanced take into consideration the unique properties of the afferent arteriolar myogenic response that allow it to protect against the oscillating systolic pressure and the accruing evidence that when this response is impaired, the primary consequence is not a disturbed volume homeostasis but rather an increased susceptibility to hypertensive injury. It is suggested that redundant and compensatory mechanisms achieve volume regulation, despite considerable fluctuations in distal delivery, and the assumed moment-by-moment regulation of renal hemodynamics is questioned.
Evidence is
Rodger Loutzenhiser,1 Karen Griffin,2
Geoffrey Williamson,3 and Anil Bidani2
1Smooth Muscle Research Group, University of
Calgary, Alberta, Canada; 2Department of
Internal Medicine, Loyola University Medical
Center and Edward Hines, Jr. Veterans Affairs
Hospital, Maywood, Illinois; and 3Department of
Electrical and Computer Engineering, Illinois
Institute of Technology, Chicago, Illinois
ABSTRACT
When the kidney is subjected to acute increases in blood pressure (BP), renal blood flow (RBF) and glomerular filtration rate (GFR) are observed to remain relatively constant. Two mechanisms, tubuloglomerular feedback (TGF) and the myogenic response, are thought to act in concert to achieve a precise moment-by-moment regulation of GFR and distal salt delivery. The current view is that this mechanism insulates renal excretory function from fluctuations in BP. Indeed, the concept that renal autoregulation is necessary for normal renal function and volume homeostasis has long been a cornerstone of renal physiology.
This article presents a very different view, at least regarding the myogenic component of this response. We suggest that its primary purpose is to protect the kidney against the damaging effects of hypertension. The arguments advanced take into consideration the unique properties of the afferent arteriolar myogenic response that allow it to protect against the oscillating systolic pressure and the accruing evidence that when this response is impaired, the primary consequence is not a disturbed volume homeostasis but rather an increased susceptibility to hypertensive injury. It is suggested that redundant and compensatory mechanisms achieve volume regulation, despite considerable fluctuations in distal delivery, and the assumed moment-by-moment regulation of renal hemodynamics is questioned.
Evidence is