Renal sympathetic nerve activity during cardiac ischemia and reperfusion in rats

We studied the role played by prostaglandins and oxygen-derived free radicals in mediating reflex changes in renal sympathetic nerve activity (RSNA) during myocardial ischemia and reperfusion. Ligation of the left coronary artery for 20 min and reperfusion for 10 min were performed in anesthetized rats with sinoaortic denervation and with intact cardiac afferent nerves (control, n = 7), with cardiac sympathetic denervation (SD, n = 6), with vagal denervation (VD, n = 7), and with combined SD +/- VD (n = 6). In control rats, RSNA decreased by 10 +/- 3% from baseline (P < 0.05) during the first minute of ischemia and increased above baseline after 5 min of ischemia, with the maximum increase at the first minute of reperfusion. In rats with SD, RSNA decreased by 19 +/- 4% from baseline (P < 0.05) at the first minute of ischemia and remained depressed during the entire ischemic and reperfusion periods. In rats with VD, RSNA increased by 26 +/- 5% from baseline (P < 0.05) at the first minute of ischemia, and the increase in RSNA at the end of the ischemic period and at reperfusion was greater than in control rats. No changes in RSNA during ischemia and reperfusion were observed with combined SD + VD. Reflex changes in RSNA that occurred at the onset of ischemia in both VD (n = 7) and SD (n = 7) rats were abolished by indomethacin (5 mg/kg iv, 20 min before ischemia). Reflex changes in RSNA after prolonged ischemia (>10 min) and during reperfusion in both VD (n = 7) and SD (n = 7) rats were abolished by the antioxidant deferoxamine (20 mg/kg iv, 20 min before ischemia). Deferoxamine also diminished the increase of RSNA at the onset of ischemia in VD rats. Thus, in rats, the vagal afferent reflex predominates during early ischemia and the sympathetic afferent reflex predominates during prolonged ischemia and reperfusion. Reflex changes in RSNA that occur at the onset of ischemia are mediated by activation of vagal and sympathetic afferent endings by prostaglandins. Reflex changes in RSNA after prolonged ischemia and during reperfusion are mediated by activation of vagal and sympathetic afferent endings by oxygen-derived free radicals.