Impotency and erectile dysfunction are common complications of heart failure. The paraventricular nucleus (PVN) of the hypothalamus is known to be involved in centrally mediated penile erection. N-methyl-D-aspartic acid (NMDA)-induced erection, yawning and stretch through the PVN can be blocked by prior administration of NO synthase (NOS) blocker, L-NMMA, in freely moving, conscious male normal rats. This study was designed to examine the role of nitric oxide (NO) within the central nervous system component of the behavioral responses including erection in rats with heart failure. The left coronary ligation-induced heart failure and sham-operated rats were used. Six to eight weeks after coronary ligation surgery, NMDA-induced erection responses through the PVN are significantly blunted in rats with heart failure compared to control rats. Concomitantly, examination of NO synthase, the enzyme responsible for the synthesis/release of NO, revealed a reduced number of NADPH diaphorase stained cells, marker of NOS activity, in the PVN of rats with heart failure compared to sham-operated control rats. Furthermore, examination of nNOS protein by Western blot analysis indicated a reduced amount of nNOS protein in the PVN of rats with heart failure compared to sham-operated control rats. These data suggest that a blunted NO mechanism in the PVN may contribute to impotence and erectile dysfunction observed in patients with heart failure.