Circulating relaxin acts on su to stimulate water driinkg i

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secretion. We mapped the sites in the brain that are activated by i.v. infusion of a dipsogenic dose of relaxin (25 tig/h) by immu- w; nohistochemically detecting Fos expression. Relaxin administra- to tion resulted in increased Fos expression in the subfornical organ O (SFO), organum vasculosum of the lamina terminalis (OVLT), me- bc dian preoptic nucleus, and magnocellular neurons in the supraoptic ot and paraventricular nuclei. Ablation of the SFO abolished relaxin- de induced water drinking, but did not prevent increased Fos expres- or sion in the OVLT, supraoptic or paraventricular nuclei. Although el ablation of the OVLT did not inhibit relaxin-induced drinking, it did br cause a large reduction in Fos expression in the supraoptic nucleus ac and posterior magnocellular subdivision of the paraventricular SI nucleus. In vitro single-unit recording of electrical activity of neu- se rons in isolated slices of the SFO showed that relaxin (10-7 M) th added to the perfusion medium caused marked and prolonged to increase in neuronal activity. Most of these neurons also re- la sponded to 10-7 M angiotensin II. The data indicate that blood- nc borne relaxin can directly stimulate neurons in the SFO to initiate stl water drinking. It is likely that circulating relaxin also stimulates re neurons in the OVLT that influence vasopressin secretion. These two circumventricular organs that lack a blood-brain barrier may have regulatory influences on fluid balance during pregnancy in Ar rats. st] ar

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