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Volume 17, Number 21,
Issue of November 1, 1997
pp. 8283-8292
Copyright ©1997 Society for Neuroscience
Angiotensin II AT1A Receptor mRNA Expression Is
Induced by Estrogen-Progesterone in Dopaminergic Neurons of the Female
Rat Arcuate Nucleus
Received June 16, 1997; revised Aug. 11, 1997; accepted Aug. 20, 1997.
Olaf Jöhren,
Gilberto L. Sanvitto,
Giorgia Egidy, and
Juan M. Saavedra
Section on Pharmacology, National Institute of Mental Health,
Bethesda, Maryland 20892
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
AT1 receptors and AT1A receptor mRNA expression increase selectively in the dorsomedial arcuate nucleus of
17 -estradiol-primed ovariectomized rats after treatment with
progesterone. In hormone-treated rats, arcuate nucleus AT1A
receptor mRNA expression is associated with tyrosine
hydroxylase-positive neurons. No AT1A receptor 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
AT1 receptors and AT1B receptor mRNA expression are decreased in 17-estradiol/progesterone-treated ovariectomized rats.
Thus, AT1A receptors in the dorsal arcuate nucleus and
AT1B receptors 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 AT1A receptor 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.
Key words:
angiotensin II receptors;
catecholamines;
tyrosine hydroxylase;
in situ hybridization;
anterior
pituitary;
prolactin
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