Endogenous noradrenaline impairs the prostaglandin-induced inhibition of noradrenaline release

Summary The effects of prostaglandin E₂ (PGE₂) on electrically evoked noradrenaline release in rat brain cortex were studied under conditions under which autoinhibition of release was avoided. When stimulation was carried out with 36 pulses at 3 Hz, 1 mol/1 PGE2, produced about 50% inhibition of release. In the presence of the ₂-adrenoceptor antagonist yohimbine (1 gmol/1) the effect of PGE₂ was markedly increased. When release was elicited by 3 pulses/100 Hz the period of stimulation was too short to permit development of autoinhibition by released noradrenaline. Then the concentration-response-curve for PGE₂ was very similar to that obtained under the above conditions (36 pulses/3 Hz, in the presence of yohimbine). These data suggest that both the ₂-adrenoceptor and the PGE₂-receptor are linked to a common pathway. Since indometacin (10 mol/1) did not enhance evoked transmitter release, an influence of endogenous PG's on in vitro release of noradrenaline from rat brain cortex slices can be excluded.Abbreviation PG prostaglandinSend offprint requests to C. Allgaier at the above address