Angiotensin II AT1A receptor mRNA expression is induced by estrogen–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 [125I]Sar1–Ang II binding to AT1receptors and AT1Areceptor mRNA expression increase selectively in the dorsomedial arcuate nucleus of 17β-estradiol-primed ovariectomized rats after treatment with progesterone. In hormone-treated rats, arcuate nucleus AT1Areceptor mRNA expression is associated with tyrosine hydroxylase-positive neurons. No AT1Areceptor mRNA was detected in tyrosine hydroxylase-positive cells of the arcuate nucleus of intact male rats. Conversely, in the anterior pituitary, where local or circulating Ang II stimulates prolactin release, [125I]Sar1–Ang II binding to AT1receptors and AT1Breceptor mRNA expression are decreased in 17β-estradiol/progesterone-treated ovariectomized rats.Thus, AT1Areceptors in the dorsal arcuate nucleus and AT1Breceptors in the anterior pituitary are regulated inversely by estrogen/progesterone treatment, supporting the hypothesis of a dual role for brain and pituitary Ang II on prolactin release. The colocalization of AT1Areceptor mRNA and tyrosine hydroxylase in neurons of the arcuate nucleus furthermore indicates that within this area central Ang II acts directly on dopaminergic neurons. These results support the hypothesis that central Ang II inhibits pituitary prolactin release indirectly via modulation of dopaminergic activity in the arcuate nucleus.