Interleukin-1 (IL-1) stimulates arginine vasopressin (AVP) release from superfused rat hypothalamo-neurohypophyseal complexes independently of cholinergic mechanism

We studied whether interleukin-1 (IL-1) affects the release of arginine vasopressin (AVP) from the superfused hypothalamo-neuropophyseal complex (HNC) of rats. Involvement of the cholinergic system in the mediation of IL-1 on AVP release from HNC was also examined. Both human recombinant IL-1α and 1β elicited a rapid increase of AVP from HNC in a dose-dependent manner at concentrations ranging from 0.1 to 10 nM. However, neither IL-1α nor -1β at concentrations of 100 nM increased AVP, and even suppressed the stimulatory effect of 10 nM IL-1α and -1β added later. Acetylcholine at concentrations of 1 to 100 nM caused a dose-dependent, rapid increase in AVP, whereas AVP release induced by 10 nM acetylcholine was completely suppressed by the combined presence of 10 μM hexamethonium, a nicotinic receptor antagonist, and 50 μM atropine, a muscanic receptor antagonist. On the other hand, AVP release induced by 10 nM IL-1α and -1β was not affected by the combination of the two agonists. These results suggest that both IL-1α and -1β may stimulate AVP release by acting directly on the hypothalamo-neurohypophyseal system, and that the stimulatory effect of IL-1 on AVP release may be independent of the cholinergic system.