PRESYNAPTIC MODULATION
NE can regulate its own release, by stimulating presynaptic, inhibitory α2-adrenergic receptors.18,19 Other inhibitors of NE release that appear to act presynaptically include ACh,20 DA, prostaglandins of the E series,21 histamine, and purines. Stimulatory modulators include angiotensin II22 and EPI, the latter of which appears to stimulate presynaptic β2-adrenergic receptors. Substantial clinical evidence supports modulation of NE release by α2-adrenoceptors.23 The roles of the other endogenous compounds remain less well established.