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Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha, Nebraska 68198-4575
The aim of the
present study was to test the hypothesis that a decrease in central
nitric oxide (NO) is involved in the enhancement of the central gain of
the cardiac "sympathetic afferent" reflex (CSAR) in dogs with
congestive heart failure (CHF). Thirteen dogs with pacing-induced CHF
and sixteen sham dogs were anesthetized with
-chloralose and were
baroreceptor denervated and vagotomized. The CSAR was evoked by
stimulation of the left ventral ansa. A lateral cerebroventricular
cannula was inserted to deliver sodium nitroprusside (SNP) and
NG-nitro-L-arginine methyl ester
(L-NAME). Arterial pressure,
heart rate, and renal sympathetic nerve activity (RSNA) were recorded at baseline and during elicitation of the CSAR. We found that 1) the responses of RSNA to
stimulation were augmented in dogs with CHF,
2) SNP depressed the increase in
RSNA induced by the CSAR in CHF dogs but had no effect in sham dogs,
and 3)
L-NAME potentiated the
CSAR-induced increase in RSNA in sham dogs but not in dogs with CHF. We
conclude that reduced central NO is involved in the enhanced central
gain of the CSAR in CHF dogs.
sodium nitroprusside; NG-nitro-L-arginine methyl ester; brain; nitric oxide synthase; renal sympathetic nerve activity
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