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The Brain Renin-Angiotensin System and Prolactin Secretion in the Male Rat^*

Department of Psychology, CSU, Stanislaus Turtock, California 95380;
Department of Physiology (M.K.S.), University of California San Francisco, California 94143-0444

Address all correspondence and requests for reprints to: Dr. Lin S. Myers, Department of Psychology, CSU, Stanislaus, 801 West Monte Vista Avenue, Turlock, California 95380.

Abstract

The present studies investigated the role of the brain renin-angiotensin system in the regulation of PRL secretion in the male rat. Blood samples were taken from conscious rats before, during, and after administration of test substances into the third cerebral ventricle. In the first series of experiments, we determined the sensitivity of the PRL response to intracerebroventrieular (icv) administration of angiotensin II (Ang II) and found that PRL levels were significantly suppressed in a dose-related manner (10–500 ng). A dose of 1 ng did not significantly affect PRL values, compared to those from vehicleinjected animals. Ang II elicited water intake at doses of 50 and 500 ng, but not at the 10- or 1-ng doses.

In the second series of experiments, we investigated the role of endogenous brain Ang II in the regulation of PRL secretion under basal and stimulated conditions. The endogenous system was manipulated by icv infusion of saralasin, an Ang II receptor antagonist, or icv injection of enalaprilat, a converting enzyme inhibitor, to prevent synthesis of Ang II. Neither saralasin nor enalaprilat administration produced an increase in PRL levels under basal, nonstressed conditions. However, during immobilization stress, when PRL levels increased 3-fold during icv vehicle infusion, saralasin infusion resulted in a 7-fold rise in plasma PRL titers relative to prestress baseline values.

These results demonstrate that, in male rats, the inhibitory effects of icv administration of Ang II on PRL secretion are very sensitive and are observed at doses which do not affect water intake. The endogenous brain Ang II system appears not to be involved in the maintenance of the low plasma PRL levels observed under basal, nonstressed conditions. However, the system does appear to affect the magnitude of the PRL response to immobilization stress, (Endocrinology 129: 1744–1748, 1991)

Footnotes

^* This study was supported by NIH Grants DK-07265, HD-28020, and HL-29714.

Received January 4, 1991.

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