Abstract
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 alpha-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.
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