Intravenous cyclosporine activates afferent and efferent renal nerves and causes sodium retention in innervated kidneys in rats.

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Abstract
The effect of acute intravenous infusion of cyclosporine (10 mg/kg) on efferent renal and genitofemoral nerve activity and afferent renal nerve activity was studied in anesthetized rats. All animals were studied after unilateral renal denervation and extracellular fluid volume expansion. Activity of both efferent sympathetic nerves was increased significantly by cyclosporine infusion (renal, 69%; genitofemoral, 60%). Afferent renal nerve activity was increased 82% after cyclosporine (P < 0.05). Urine flow rate and both absolute and fractional sodium excretion from the innervated kidney were reduced 50% after cyclosprine infusion (P < 0.01). Absolute and fractional sodium excretion from the denervated kidney were significantly increased after after cyclosporine. Infusion of vehicle had no significant effect on any measured variable in innervated or denervated kidneys. These studies demonstrate the capacity of cyclosporine to increase efferent sympathetic nerve activity and afferent nerve activity. It is also shown that sodium retention resulting from acute infusion of cyclosporine can be attributed to the increase in efferent renal nerve activity.