Blood pressure is well established to contain a potential oscillation betwe
en 0.1 and 0.4 Hz, which is proposed to reflect resonant feedback in the ba
roreflex loop. A linear feedback model, comprising delay and lag terms for
the vasculature, and a linear proportional derivative controller have been
proposed to account for the 0.4-Hz oscillation in blood pressure in rats. H
owever, although this model can produce oscillations at the required freque
ncy, some strict relationships between the controller and vasculature param
eters must be true for the oscillations to be stable. We developed a nonlin
ear model, containing an amplitude-limiting nonlinearity that allows for si
milar oscillations under a very mild set of assumptions. Models constructed
from arterial pressure and sympathetic nerve activity recordings obtained
from conscious rabbits under resting conditions suggest that the nonlineari
ty in the feedback loop is not contained within the vasculature, but rather
is confined to the central nervous system. The advantage of the model is t
hat it provides for sustained stable oscillations under a wide variety of s
ituations even where gain at various points along the feedback loop may be
altered, a situation that is not possible with a linear feedback model. Our
model shows how variations in some of the nonlinearity characteristics can
account for growth or decay in the oscillations and situations where the o
scillations can disappear altogether. Such variations are shown to accord w
ell with observed experimental data. Additionally, using a nonlinear feedba
ck model, it is straightforward to show that the variation in frequency of
the oscillations in blood pressure in rats (0.4 Hz), rabbits (0.3 Hz), and
humans (0.1 Hz) is primarily due to scaling effects of conduction times bet
ween species.