Sympathetic nerve activity (SNA) consists of discharges which vary in amplitude and frequency, reflecting the level of recruitment of nerve fibres and the rhythmical generation and entrainment of activity by the central nervous system. It is unknown whether selective changes in these amplitude and frequency components account for organ-specific changes in SNA in response to alterations in blood volume, or for the impaired SNA responses to volume changes in heart failure (HF). To address these questions, we measured cardiac SNA (CSNA) and renal SNA (RSNA) simultaneously in conscious, normal sheep and sheep in HF, induced by rapid ventricular pacing. Volume expansion decreased CSNA (-62±10%, p<0.05) and RSNA (-59±10%, p<0.05) equally (n=6). CSNA decreased due to a reduction in burst frequency, while RSNA fell due to falls in burst frequency and amplitude. Hemorrhage increased CSNA (+74±9%, p<0.05) more than RSNA (+21±5%, p<0.09), in both cases due to increased burst frequency, whereas burst amplitude decreased. In HF, burst frequency of CSNA (26±3 to 75±3 bursts/min) increased more than that of RSNA (63±4 to 79±4 bursts/min). In HF, volume expansion caused no change in CSNA and an attenuated decrease in RSNA, due entirely to decreased burst amplitude. Hemorrhage did not significantly increase SNA in either nerve in HF. These findings support the concept that the number of sympathetic fibres recruited and their firing frequency are controlled independently. Furthermore, afferent stimuli, such as changes in blood volume, cause organ-specific responses in each of these components, which are also selectively altered in HF.