ANGIOTENSIN-II AT(1A) RECEPTOR MESSENGER-RNA EXPRESSION IS INDUCED BYESTROGEN-PROGESTERONE IN DOPAMINERGIC-NEURONS OF THE FEMALE RAT ARCUATE NUCLEUS

Brain angiotensin II (Ang II) inhibits pituitary prolactin release by an indirect mechanism requiring stimulation of dopamine formation and release. We report that [I-125]Sar(1)-Ang II binding to AT(1) receptor s and AT(1A) receptor mRNA expression increase selectively in the dors omedial arcuate nucleus of 17 beta-estradiol-primed ovariectomized rat s after treatment with progesterone. In hormone-treated rats, arcuate nucleus AT(1A) receptor mRNA expression is associated with tyrosine hy droxylase-positive neurons. No AT(1A) receptor mRNA was detected in ty rosine hydroxylase-positive cells of the arcuate nucleus of intact mal e rats. Conversely, in the anterior pituitary, where local or circulat ing Ang II stimulates prolactin release, [I-125]Sar(1)-Ang II binding to AT(1) receptors and AT(1B) receptor mRNA expression are decreased i n 17 beta-estradiol/progesterone-treated ovariectomized rats. Thus, AT (1A) receptors in the dorsal arcuate nucleus and AT(1B) receptors in t he anterior pituitary are regulated inversely by estrogen/progesterone treatment, supporting the hypothesis of a dual role for brain and pit uitary Ang II on prolactin release. The colocalization of AT(1A) recep tor mRNA and tyrosine hydroxylase in neurons of the arcuate nucleus fu rthermore indicates that within this area central Ang II acts directly on dopaminergic neurons. These results support the hypothesis that ce ntral Ang II inhibits pituitary prolactin release indirectly via modul ation of dopaminergic activity in the arcuate nucleus.