Systolic blood pressure as the trigger for the renal myogenic response: protective or autoregulatory?
OBJECTIVE
The ability of the kidney to autoregulate renal blood flow and glomerular filtration rate has long been viewed as existing to prevent fluctuations in blood pressure from causing parallel fluctuations in renal function and distal delivery of filtrate. This review, however, points out that the primary consequence of the loss of this autoregulatory capacity is not a disturbance in volume regulation, but rather an increased susceptibility to hypertensive injury. Moreover, the kinetic requirements for renal protection indicate that current views of dynamic autoregulation cannot explain how the kidney is normally protected against acute elevations in systolic blood pressure.


RESULTS
Recent findings suggest that the kinetics of the myogenic mechanism of the afferent arteriole are uniquely suited to protect against acute elevations in the systolic blood pressure, in that this vessel not only senses this rapidly oscillating blood pressure component, but that its response is exclusively dependent on this signal.


CONCLUSIONS
These new findings are consistent with recent data indicating that it is the systolic blood pressure elevations that most closely correlate with target organ damage. The fact that the myogenic mechanism is also a necessary component of renal autoregulation may explain the strong linkage between autoregulatory impairment and increased susceptibility to hypertensive injury.
Loutzenhiser
Rodger
R
Smooth Muscle Research Group, Department of Pharmacology and Therapeutics, University of Calgary Faculty of Medicine, 3330 Hospital Drive NW, Calgary, Alberta T2N 4N1, Canada. rloutzen@ucalgary.ca
Griffin
Karen A
KA
Bidani
Anil K
AK
D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D005919:Glomerular Filtration Rate / Q000502:physiology*; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply / Q000502:physiology*; D051381:Rats; D014661:Vasoconstriction / Q000502:physiology