[Angiotensin II release and anti-electroacupuncture analgesia in spinal cord]

Changes in the content of angiotensin II (A II) immunoreactivity (ir) in rat spinal perfusate induced by electroacupuncture (EA) stimulation of different frequencies were measured by radioimmunoassay (RIA). The results were analyzed in relation to the role of opioid receptor. (1) 2 Hz EA produced a 20% (P > 0.05) decrease in A II -ir content in the spinal perfusate. 15 Hz EA produced an even more decrease (62%, P < 0.01), whereas 100 Hz produced a significant increase (65%, P < 0.05). (2) The release in spinal A II -ir produced by 15 Hz EA was reversed by the opioid antagonist naloxone to a of 125% highter than that of the control (P < 0.05), suggesting that 15 Hz EA may accelerate the release of endogenous opioids to suppress the release of A II. (3) This was substantiated by the finding that intrathecal (i.t.) injection of the selective mu agonist ohmefentanyl produced a dramatic suppression (20%, P < 0.05) of A II release, but not by delta and kappa agonist. (4) Intrathecal injection of salarasin, the angiotensin receptor antagonist, produced a significant potentiation of the analgesia produced by 100 Hz EA, but not that produced by 2 or 15 Hz EA. It is concluded that 15 Hz EA may induce the release of endogenous opioids acting on mu opioid receptor so as to suppress A II release, and that 100 Hz EA may accelerate the release of A II serving as a brake for 100 Hz EA-induced analgensia. Removal of the brake by angiotensin antagonist may be advised as an adjunct for the potentiation of 100 Hz EA-induced analgesia.