Renal autoregulation maintains stable renal blood flow in the face of constantly fluctuating blood pressure.
Autoregulation is also the only mechanism that protects the delicate glomerular capillaries when blood pressure increases.
In order to understand autoregulation, the renal blood flow response to changing blood pressure is studied. The steadystate
response of blood flow is informative, but limits investigation of the individual mechanisms of autoregulation. The
dynamics of autoregulation can be probed with transfer function analysis. The frequency-domain analysis of autoregulation
allows investigators to probe the relative activity of each mechanism of autoregulation. We discuss the methodology
and interpretation of transfer function analysis. Autoregulation is routinely studied in the rat, of which there are many inbred
strains. There are multiple strains of rat that are either selected or inbred as models of human pathology. We discuss
relevant characteristics of Brown Norway, Spontaneously hypertensive, Dahl, and Fawn-Hooded hypertensive rats and
explore differences among these strains in blood pressure, dynamic autoregulation, and susceptibility to hypertensive renal
injury. Finally we show that the use of transfer function analysis in these rat strains has contributed to our understanding
of the physiology and pathophysiology of autoregulation and hypertensive renal disease.Interestingly all these strains
demonstrate effective tubuloglomerular feedback suggesting that this mechanism is not sufficient for effective autoregulation.
In contrast, obligatory or conditional failure of the myogenic mechanism suggests that this component is both necessary
and sufficient for autoregulation.
Keywords: Autoregulation, blood pressure, dynamics, rats, inbred BN rats, inbred Dahl rats, fawn-hooded hypertensive rats,
inbred SHR, renal blood flow.
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