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The aim of the study was to evaluate the influence of renal sympathetic nerves on the production of interleukin (IU-6 in the kidney of normotensive Wistar rats and spontaneously hypertensive rats (SHR).In acute studies, the left kidney was exposed and the renal nerves were electrically stimulated to decrease renal blood flow by either 15 or 30% for 1 h. The changes in renal function induced by nerve stimulation were measured and IL-6 production estimated at the end of the experiment.Pentobarbitone anaesthetized rats were prepared for the measurement of renal blood flow, glomerular filtration rate and water and sodium excretion. IL-6 production was estimated by the level of IL-6 messenger (m)RNA present in the kidney tissue.At the lower level of nerve stimulation there were reductions in the glomerular filtration rate of 12 and 24% in Wistar and SHR, respectively, and a decrease in sodium excretion of approximately 30% in both rat strains. At higher rates of stimulation these haemodynamic and tubular responses were proportionately larger. The mRNA for IL-6 and P-actin were measured by densitometric analysis of Northern blot gels following hybridization. Renal IL-6 mRNA levels in the Wistar rat demonstrated that the gene was actively expressed and was increased some threefold by renal nerve stimulation. By contrast, IL-6 mRNA was extremely low in SHR compared with that found in the kidneys of Wistar rats and did not appear to be changed by renal nerve stimulation.These findings suggest that the renal sympathetic nerves are an important regulatory mechanism for IL-6 production under normal conditions. However, in the SHR, production of IL-6 in the kidney appears to be suppressed.