Renal ischemia enhances electrical activity and Fos protein expression of the rostral ventrolateral medullary neurons in rats.

The effects of renal ischemia on spontaneous electrical activity and Fos protein expression of nucleus paragigantocellularis lateralis (PGL) in rostral ventrolateral medulla (RVLM) were observed in 67 anesthetized Sprague-Dawley rats with sinoaortic denervation by using extracellular recording and immunohistochemical techniques. The results obtained are as follows. (1) Renal ischemia increased the discharge rate from 11.40 +/- 1.08 to 21.1 +/- 1.74 spikes/s (P < 0.001) in 28 out of 30 PGL neurons, while blood pressure and heart rate had no significant change (P > 0.05). (2) Administration of 8-phenyltheophylline (8-PT), an adenosine receptor antagonist, did not affect the discharge rate of PGL neurons, but could partially inhibit the effects of renal ischemia in 17 units (P < 0.05). (3) Renal ischemia resulted in a remarkable increase in the number of Fos-like protein immunoreactive PGL neurons in the RVLM (P < 0.01). (4) Fos protein expression induced by renal ischemia was significantly inhibited by pretreatment with 8-PT (P < 0.05). Taken together, it is concluded that renal ischemia induces an increase in spontaneous electrical activity and Fos protein expression in PGL neurons of RVLM, and that adenosine released within ischemic kidney may be involved in such effects.