The Dahl salt-sensitive (Dahl S) rat develops hypertension and renal i
njuries when challenged with a high salt diet and has been considered
to be a model of chronic renal failure. Renal injuries appear very ear
ly in life compared with the spontaneously hypertensive rat (SHR). Dur
ing the course of hypertension, a gradual impairment of autoregulatory
control of renal blood flow might expose the glomerular circulation t
o periods of elevated pressure, resulting in renal injuries in Dahl S
rats. Dynamic autoregulatory capacity was assessed in Dahl S and Dahl
salt-resistant (Dahl R) rats, SHR, and Sprague-Dawley rats by inducing
broad-band fluctuations in the arterial blood pressure and simultaneo
usly measuring renal blood flow. Dynamic autoregulation was estimated
by the transfer function using blood pressure as the input and renal b
lood flow as the output. Renal morphological injuries were evaluated i
n Dahl S rats and SHR and were scored semiquantitatively. Dynamic auto
regulation was efficient and comparable in the low-frequency range (<0
.015 Hz) in Dahl R rats, SHR, and Sprague-Dawley rats. The response in
Dahl S rats depended strongly on the initiation time of the high salt
diet. Autoregulation was preserved during a low salt diet and in rats
exposed to a late-onset hypertension of short duration, only partly p
reserved if the late-onset hypertension was of a longer duration, and
abolished in early-onset hypertension. All Dahl S rats on a high salt
diet showed severe morphological changes in the kidney. In conclusion,
autoregulatory capacity in the kidney of Dahl S rats is gradually imp
aired when rats are rendered hypertensive with a high salt diet. Renal
morphological injuries develop before loss of dynamic autoregulation.
Impaired autoregulation appears to be the result, not the cause, of t
he process that ultimately leads to renal failure in the Dahl S rat.