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Do Baroreflexes Play a Role in Long-Term Control of Arterial
Pressure?
APS Water & Electrolyte Homeostasis Section
Thomas E. Lohmeier
T.E. Lohmeier, S.C. Malpas, J.W. Osborn and T.N. Thrasher
There is considerable evidence that the sympathetic nervous system plays
an important role in the pathogenesis of hypertension (and heart failure).
However, the factors that chronically influence sympathetic activity and the
precise mechanisms that mediate neurally induced hypertension are unclear.
In large part, this has been due to technical limitations that prevent
assessment of sympathetic function under chronic conditions. An area of
long-standing interest, but one of considerable uncertainty, relates to the
potential impact of baroreflexes on sympathetic activity and arterial
pressure in chronic hypertension. Clearly, baroreflex function is often
impaired in chronic hypertension, but whether baroreflex dysfunction
contributes to increased sympathetic activity and the severity of
hypertension is unresolved.
As baroreflexes reset in the direction of the prevailing level of
arterial pressure, a popular notion is that they play little role in
long-term regulation of arterial pressure. Consequently, one contention is
that baroreflexes have little impact on the severity of hypertension. On
the other hand, recent studies in chronically instrumented animals using
novel experimental approaches have clearly demonstrated that baroreflexes
are chronically activated in hypertension. However, the quantitative
importance of baroreflexes in attenuating the severity of different forms of
hypertension and the mechanisms whereby suppression of sympathetic activity
chronically reduces arterial pressure are unclear. Recent studies in
chronically instrumented animals indicate that baroreflexes chronically
suppress renal sympathetic activity and promote sodium excretion in
hypertension. As alterations in renal excretory function play a critical
role in long-term regulation of arterial pressure, these studies suggest
that baroreflex suppression of renal sympathetic nerve activity may be an
important mechanism for attenuating the severity of hypertension. While
inconsistent with this hypothesis, another possibility is that reductions in
sympathetic activity to non-renal vascular beds also contributes to the
chronic blood pressure lowering effects of baroreflex activation. This
symposium will present experimental evidence relating to these fundamental
hypotheses.
The speakers and Chairs of this symposium are researchers expert in
chronic experimental paradigms, and in integrative CV physiology. A goal
will be to identify the important questions that will drive research in the
area. The speakers will provide their own perspective as to whether
baroreflexes play a role in long-term control of arterial pressure and, if
so, how this response is achieved.
This symposium will be of interest to both basic scientists and
clinicians interested in the determinants of sympathetic activity,
particularly in the disease states of hypertension and heart failure, and
the neuroendocrine mechanisms whereby alterations in sympathetic activity
alter renal excretory function and arterial pressure. A particularly
important aim of this symposium will be to focus on the impact of
neuroendocrine mechanisms on renal excretory function and how alterations in
baroreflex activity lead to chronic changes in arterial pressure. This
important topic has not been specifically covered at previous meetings.
Neural mechanisms in cardiovascular regulation, including the role of
baroreflexes, are covered in regular EB meetings and at FASEB summer
conferences, but the focus is on short-term control of blood pressure. As
such, the information from these meetings may or may not be relevant to
mechanisms of long-term blood pressure control.
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