Evidence for prostaglandin mediated prejunctional control of renal sympathetic transmitter release and vascular tone.

1 Prostaglandin E(2) dose-dependently and reversibly inhibited the noradrenaline overflow resulting from nerve stimulation of the rabbit kidney.2 The magnitude of this inhibition varied inversely with the frequency of stimulation employed.3 The prostaglandin synthesis inhibitors, indomethacin and meclofenamic acid, both increased the transmitter overflow resulting from renal nerve stimulation, suggesting that endogenous prostaglandin has a role in the regulation of transmitter release.4 In the presence of indomethacin, the inhibitory effect of exogenous prostaglandin E(2) was enhanced.5 The prostaglandin precursor, arachidonic acid, also caused a significant, dose-dependent and reversible inhibition of transmitter overflow. This inhibition became insignificant when arachidonic acid was applied in the presence of indomethacin, suggesting that the inhibition was mediated by newly formed prostaglandin rather than by arachidonic acid itself.6 It is proposed that newly formed prostaglandin controls noradrenaline release primarily from inner cortical nerve endings, thereby maintaining juxtamedullary blood flow under periods of increased sympathetic nerve activity.