Effects of methylprednisolone on renal nerve response to stimulation of medullary pressor area in endotoxin-induced hypotension.

The purpose of this study was to determine the effects of glucocorticoids on central sympathetic outflow during endotoxic hypotension in anesthetized rabbits. All animals were given E. coli endotoxin (1 mg/kg) intravenously. In the control group, mean blood pressure (MBP) fell significantly after endotoxin. Endotoxin also caused a significant reduction of renal nerve activity (NA) simultaneously with a decrease in MBP. Peak responses in MBP and NA to repetitive stimulation of the medullary pressor area were attenuated significantly 60 min after endotoxin. Both peak and total activities of renal nerve discharges (RNDe) evoked by the electrical stimulation of the medullary pressor area were significantly reduced. There were no significant differences in the time course changes in the above parameters between the control group and the treated group. Following a vehicle injection in the control group, these parameters decreased by endotoxin progressively declined until the end of the experiment. When methylprednisolone (MPSS, 30 mg/kg) was injected intravenously 60 min after endotoxin, decreases in MBP and NA induced by endotoxin recovered gradually toward preendotoxin levels. Thirty minutes after MPSS administration levels of MBP and NA were significantly higher than those in the control group. Responsiveness in MBP and NA to the repetitive stimulation of the medullary pressor area increased significantly after the treatment with MPSS. Peak activities of RNDe 30 min after MPSS were augmented significantly and total activities of RNDe recovered to preendotoxin levels. Both endotoxin and MPSS did not affect MBP, NA, and RNDe responses following stimulation of the thoracic sympathetic chain. These findings suggest that methylprednisolone may have improved the impaired central blood pressure regulatory circuits during endotoxic hypotension through a facilitation of neuronal excitability, resulting in an enhancement of central sympathetic outflow.