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1 Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha, Nebraska 68198 - 4575; and 2 Merck Research Laboratories, West Point, Pennsylvania 19486
Endothelin-1 (ET-1) is elevated in
chronic heart failure (CHF). In this study, we determined the effects
of chronic ET-1 blockade on renal sympathetic nerve activity (RSNA) in
conscious rabbits with pacing-induced CHF. Rabbits were chronically
paced at 320-340 beats/min for 3-4 wk until clinical and
hemodynamic signs of CHF were present. Resting RSNA and arterial
baroreflex control of RSNA were determined. Responses were determined
before and after the ET-1 antagonist L-754,142 (a combined
ETA and ETB receptor antagonist,
n = 5) was administered by osmotic minipump infusion (0.5 mg · kg
1 · h1 for
48 h). In addition, five rabbits with CHF were treated with the
specific ETA receptor antagonist BQ-123. Baseline RSNA
(expressed as a percentage of the maximum nerve activity during sodium
nitroprusside infusion) was significantly higher (58.3 ± 4.9 vs.
27.0 ± 1.0, P < 0.001), whereas baroreflex
sensitivity was significantly lower in rabbits with CHF compared with
control (3.09 ± 0.19 vs. 6.04 ± 0.73, P < 0.001). L-754,142 caused a time-dependent reduction in arterial
pressure and RSNA in rabbits with CHF. In addition, BQ-123 caused a
reduction in resting RSNA. For both compounds, RSNA returned to near
control levels 24 h after removal of the minipump. These data
suggest that ET-1 contributes to sympathoexcitation in the CHF state.
Enhancement of arterial baroreflex sensitivity may further contribute
to sympathoinhibition after ET-1 blockade in heart failure.
baroreflex; ET receptors; autonomic nervous system; myocardial dysfunction; neurohormones
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