J Neuroendocrinol. 1989 Aug 01;1(4):299-303. doi: 10.1111/j.1365-2826.1989.tb00119.x.

The brain Renin-Angiotensin system and the regulation of prolactin secretion in female rats: influence of ovarian hormones.

Journal of neuroendocrinology

L S Myers, M K Steele

PMID: 19210444 DOI: 10.1111/j.1365-2826.1989.tb00119.x

Abstract

Abstract This study was designed to investigate the effects of exogenous and endogenous angiotensin II (All) on prolactin release in ovariectomized rats, with and without estrogen and progesterone pretreatment. In the first series of experiments, All or vehicle was injected into the third cerebral ventricle of conscious, freely-moving rats. In both treated and untreated rats, administration of 50 ng All suppressed prolactin levels within 15min of injection, compared to vehicle-injected rats. In untreated rats, prolactin levels returned to baseline values by 30 min, while in treated rats, prolactin levels remained suppressed for an hour. In the second series of experiments, the involvement of endogenous brain All in tonically suppressing prolactin release was assessed by administering either All receptor blockers (saralasin or sarthran) or an All synthesis inhibitor (enalaprilat, an inhibitor of the conversion of angiotensin I to All). Neither All receptor blockade nor converting enzyme inhibition resulted in any change in prolactin levels in untreated levels in untreated rats. However, following treatment with ovarian steroids, infusion of saralasin or injection of enalaprilat resulted in a significant increase in plasma prolactin tilers. During saralasin infusion, prolactin levels were significantly increased by 15 min and continued to be higher than controls at 60 min. After enalaprilat administration, prolactin levels did not rise significantly until 90 min and then remained elevated up to 120 min post-injection. These latter results suggest that at least one h is required for maximal inhibition of angiotensin synthesis in the brain. These data demonstrate that low doses of All suppressed basal prolactin secretion in both untreated and ovarian steroid-treated, ovariectomized rats. However, treated rats appeared to be more sensitive than untreated animals to the prolactin-lowering effects of centrally administered All. The lack of prolactin response in untreated rats when brain All synthesis was inhibited or All receptors were blocked suggests that, in the absence of ovarian steroids, endogenous All was not acting tonically to suppress prolactin secretion. Following exposure to ovarian steroids, however, the endogenous brain All system appeared to be activated and involved in controlling prolactin release.

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