1. This study sets out to examine the effect of rilmenidine administered systemically on basal and reflexly activated renal nerve activity in Wistar and stroke prone spontaneously hypertensive rats (SHRSP). 2. Animals were anaesthetized with chloralose/urethane, stimulating electrodes were placed on the brachial plexi and the renal nerves were isolated and put on recording electrodes. Both brachial nerves were stimulated electrically at 0.8, 1.6 and 3.2 Hz (15 V, 0.2 ms) in the absence and in the presence of rilmenidine given at 100 and 200 micrograms kg-1 i.v. in a cumulative manner. 3. Stimulation of the brachial nerves caused graded increases in blood pressure, heart rate and integrated renal nerve activity (P < 0.05) in both Wistar and SHRSP. Fast Fourier transformation of the renal nerve activity signal to generate a power spectrum demonstrated that both total power and percentage power at heart rate was higher in the SHRSP than Wistar (P < 0.05). Total power was raised during brachial nerve stimulation in both Wistar and SHRSP by some 200-300% (P < 0.05) but the percentage power at heart rate was decreased by some 60% (P < 0.01) in the Wistar but was raised by some 40-50% (P < 0.05) in the SHRSP. 4. Administration of rilmenidine caused dose-related decreases in blood pressure and heart rate and integrated renal nerve activity in both Wistar and SHRSP (all P < 0.05). Both doses of rilmenidine decreased (P < 0.05) the total power in the signal in both strains of rat by about one-half but the power occurring at heart rate only fell at the higher dose of compound in the Wistar, whereas in the SHRSP it was decreased by both doses by approximately 60-70%. In the presence of rilmenidine, coherence of the renal nerve signal was reduced in the Wistar and SHRSP and although the drug had no effect on phase difference in the Wistar, this parameter was decreased in the SHRSP by the low and high doses of rilmenidine (P < 0.05). 5. In the presence of 100 micrograms kg-1 rilmenidine, stimulation of the brachial nerves caused increases in total power in the Wistar and SHRSP (two to three fold, P < 0.05), together with a decrease (P < 0.05) in the percentage power occurring at heart rate in the Wistar, of some 60%, and an increase (P < 0.01) in the SHRSP, of some two to three times, which were very similar in magnitude and pattern to those obtained in the absence of the drug. Following the 200 micrograms kg-1 dose of rilmenidine, brachial nerve stimulation increased total power in the Wistar and SHRSP groups (P < 0.05) and whereas in the Wistar the percentage power at heart rate did not change in the SHRSP it was again increased in response to the electrical stimulation of the brachial plexus (P < 0.001) by between two to three fold. 6. These results showed that in both the Wistar and SHRSP rilmenidine depressed blood pressure, heart rate and integrated renal nerve activity. Moreover, rilmenidine did not affect the reflex activation of renal nerve activity via the somatosensory system although the characteristics within the power spectra underwent certain changes which might have a functional impact at the level to the kidney.