Cardiac sympathetic afferent reflex in dogs with congestive heart
failure.
Wang, Wei, and Irving H. Zucker.
Department of Physiology and Biophysics, University of Nebraska
College of Medicine, Omaha, NE 68198-4575
APStracts 3:0132R, 1996.
It is well accepted that sympathetic tone is elevated in chronic heart
failure (HF) and that the cardiac sympathetic afferent reflex is a
sympathoexcitatory reflex. There have been no studies designed to to
examine the role of this reflex in control of sympathetic outflow in
the heart failure state. In this study we tested the hypothesis that
cardiac sympathetic afferent reflexes are enhanced in HF and are
therefore, capable of contributing to the increase in sympathetic
outflow in this disease state. Ventricular pacing was carried out in
14 dogs until signs of HF were evident. Fourteen sham dogs served as
controls. At the time of the acute experiment the dogs were
anesthetized with [alpha]-chloralose. The hemodynamic (arterial
pressure and heart rate) and renal sympathetic nerve (RNA) responses
to left ventricular epicardial application of two doses of bradykinin
(BK) and capsaicin (CAP) were determined in the sino-aortic
denervated and vagotomized state. The MAP, RNA and HR responses to
bradykinin were greater in the HF group compared to the sham group.
The RNA response to bradykinin (50 [mu]g) in the HF group was
significantly increased (34.0 +/- 5.9% vs. 11.5 +/- 4.2%,
p<0.05). The MAP, RNA and HR responses to capsaicin in the heart
failure group were similar to the responses to bradykinin. The RNA
response to capsaicin in the HF group was significantly increased
(29.8 +/- 11.3% vs. 13.8 +/- 2.3% for 10 [mu]g, p < 0.05 and
46.5% +/- 10.7% vs. 18.7% +/- 3.1% for 100 [mu]g, p < 0.05). The
cyclooxygenase blocker, indomethacin (5 mg/kg, iv) attenuated the
reflex responses to bradykinin in the HF group. These data suggest
that the enhanced cardiac sympathetic afferent reflex to epicardial
bradykinin in HF appears to be mediated by altered levels of
prostaglandin synthesis. Blockade of cardiac sympathetic afferents
with topical lidocaine reduced baseline of RNA significantly more in
the HF state than in the normal state (-24.2 +/- 3.6% vs. -4.3 +/-
4.5%, p<0.05). We conclude from these data that the cardiac
sympathetic afferent reflex is sensitized in the HF state and
speculate that this enhanced cardiac sympathetic afferent reflex may
contribute to the sustained higher sympathetic tone in chronic HF.
Received 3 November 1995; accepted in final form 1 April 1996.
APS Manuscript Number R684-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 16 April 96