Modulation by Dopamine and Estradiol of the Central Effects of Angiotensin II on Anterior Pituitary Hormone Release*

Abstract

The effects of iv or intraventricular (ivt) angiotensin II (All) administration on plasma levels of PRL, LH, GH, and TSH were studied in conscious ovariectomized (OVX) female rats with (and in some cases without) estradiol benzoate (Eb) priming. Both iv and ivt administration of AII increased LH levels in OVX, Eb-primed rats, but not in OVX, unprimed animals. Central All injection in OVX, Eb-primed rats induced sustained decreases in PRL and GH levels, which were reversed by pretreatment with saralasin, a specific AII receptor blocker. Systemic administration of AII in OVX, Eb-primed rats produced rapid and transient changes in PRL and GH levels. Peripheral dopaminergic receptor blockade with domperidone prevented the ivt AII-induced decline in PRL levels. Plasma levels of GH and LH were depressed after domperidone treatment, but ivt AII still induced a modest but significant decrement in GH levels. Plasma levels of TSH were not affected by either ivt or iv injection of AII Similarly, AII treatment in domperidone-treated rats was ineffective at inducing any changes in TSH levels. In another group of OVX, Eb-primed rats, AII or saline was given ivt, and the animals were killed by decapitation 15 min later. Measurement of catecholamine levels in the arcuate and median eminence regions indicated that a significant increase in dopamine (DA) levels occurred in the arcuate region. No changes in norepinephrine levels were seen in the same area, nor were the DA and norepinephrine levels in the median eminence affected by AII These results indicate that central administration of AII selectively lowers PRL and GH levels, whereas it elevates LH levels; the latter effect is seen only in the Eb-primed animals. Since the effects of All on LH are seen after both ivt and iv injection of the peptide, they may indicate, at least in part, a direct action of AII at the pituitary level to stimulate LH release. The action of AII to inhibit PRL release may, perhaps, be mediated by the tuberoinfundibular dopaminergic system, while the effects of AII on GH release do not seem to be mediated by peripheral DA receptors. The latter effect, therefore, may involve other central neurotransmitter systems or, alternatively, may reflect direct actions of All upon the somatostatin neuron.