In chloralose/urethane anaesthetised stroke-prone spontaneously hypertensive rats, blood pressure and integrated renal nerve activity were higher whereas heart rate was lower than in Wistar rats by 37, 146 and 11%, respectively (all P < 0.001). The renal nerve signal was subjected to fast Fourier transformation to generate power spectra. In the hypertensive rats, total spectral power was 400% (P < 0.01) and power at the heart rate frequency was 50% (P < 0.01) greater while phase and time differences were shorter (both P < 0.001) than in Wistar rats. Brachial nerve stimulation increased total power in Wistar and hypertensive rats (P < 0.05), but importantly, power at the heart rate frequency was decreased by 80% in Wistar whereas there was a 20% (P < 0.05) increase in hypertensive rats, while phase and time differences were raised only in hypertensive rats (P < 0.05). Bilateral cervical vagotomy of the hypertensive rats had minimal actions on most variables but phase and time differences were doubled compared to intact hypertensive animals, but brachial nerve stimulation decreased power at the heart rate frequency (P < 0.05) which was a very different response from intact rats. Resting blood pressure, heart rate, total power and power at the heart rate frequency in the carotid sinus denervated animals were lower than in intact hypertensive rats, between 17 and 71%, respectively, but increased during brachial nerve stimulation. These experiments demonstrated that whereas somatic sensory input can modulate the pattern of sympathetic nerve activity to the kidney under normal conditions, this does not occur in the hypertensive rat. This appears to be related to afferent information carried by the vagus which suppresses the normal response; the carotid sinus baroreceptors are devoted to organising the nerve activity in relation to the blood pressure pulse wave.