Noradrenaline release in rodent tissues is inhibited by interleukin-1β but is not affected by urotensin II, MCH, NPW and NPFF

We studied whether noradrenaline release is affected by interleukin-1β and the neuropeptides urotensin II, melanin-concentrating hormone (MCH), neuropeptide W (NPW) and neuropeptide FF (NPFF). Rodent tissues preincubated with [3H]noradrenaline were superfused, and the effect of peptides on the electrically-evoked tritium overflow (“noradrenaline release”) was studied. In mouse brain cortex, interleukin-1β at 0.3nM and the prostaglandin E2 analogue sulprostone at 3nM inhibited noradrenaline release by about 40%; the effect of interleukin-1β developed gradually, whereas the effect of sulprostone occurred promptly. Urotensin II at 0.001–1µM did not affect noradrenaline release in rat kidney cortex, whereas 0.01µM angiotensin II increased it (positive control). MCH at 0.01–1µM did not alter noradrenaline release in the rat brain cortex, and NPW 1µM did not affect noradrenaline release in the mouse hypothalamus or hippocampus. In each model, 0.1µM sulprostone inhibited noradrenaline release (positive control). NPFF and the NPFF2 receptor agonist dNPA (1µM) did not affect noradrenaline release in the mouse atria; the inhibitory effect of the δ opioid receptor agonist 1µM DPDPE on noradrenaline release in this tissue was not altered by NPFF or dNPA at 0.32µM but was counteracted by the δ opioid antagonist naltrindole at 0.001µM. In conclusion, interleukin-1β inhibits noradrenaline release in the mouse cortex; the effect develops gradually, suggesting that it affects protein biosynthesis. Noradrenergic neurons in various tissues from rodents are devoid of presynaptic receptors for urotensin II, MCH, NPW and NPFF. Finally, an interaction between a δ opioid agonist and NPFF could not be detected.