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Studies on Autoregulation of Prolactin Secretion from Perifused Rat Pituitary Glands in the Basal and Thyrotropin-Releasing Hormone-Stimulated States^*

BRUCE L. MALTZ, MAIRE T. BUCKMAN, GLENN T. PEAKE, EXPERT TECHNICAL ASSISTANCE and JOSEPHINE MORRIS

Medicine and Research Services, Veterans Administration Hospital, and the Department of Medicine, The University of New Mexico School of Medicine Albuquerque, New Mexico 87131

Address requests for reprints to: Dr. Maire T. Buckman, Research Service (151), Veterans Administration Hospital, 2100 Ridgecrest Drive S.E., Albuquerque, New Mexico 87131.

Abstract

In order to evaluate autoregulation of PRL secretion at the pituitary gland, spontaneous and TRH-stimulated PRL secretion was determined in an isolated anterior pituitary (AP) perifusion system utilizing normal and chronically hyperprolactinemic (MtTW 15 tumor-bearing) male rat pituitaries. Decreased AP weight in chronically hyperprolactinemic rats [5.7 ± 0.1 (SE) VS. 7.2 ± 0.2 mg in controls, P < 0.001] was associated with lower mean basal PRL secretion compared to controls (9.9 ± 1.8 vs. 20.6 ± 2.7 ng/min/AP, P < 0.01). PRL secretion from normal AP was not altered by the addition of ovine PRL (oPRL) at 10 or 100 ng/ml (19.9 ± 3.8 and 19.2 ± 2.9 ng/min/AP, respectively). TRHstimulated PRL secretion from normal AP in the absence of oPRL was 133 ± 7% of baseline (designated as 100%) and this did not differ from the response observed in the presence of 10 or 100 ng/ml oPRL (134 ± 9 and 133 ± 7%, respectively). Basal PRL secretion from tumor rat AP was likewise unaffected by the presence of medium oPRL (9.9 ± 1.8 in the absence of oPRL and 10.0 ± 1.9 ng/min/AP in the presence of 100 ng/ml oPRL). TRH-stimulated PRL secretion from tumor rat AP was 149 ± 10% of baseline in the absence of medium oPRL and 140 ± 7% in the presence of 100 ng/ml oPRL (P > 0.10). The data suggest that autoregulation of PRL secretion exists, and this regulation may not be mediated directly at the pituitary gland but rather at higher, possibly hypothalamic, centers.

Footnotes

^* This work was supported by NIH Grants HD-05794-05 and RR-00997-02.

Recipient of VA Clinical Investigator Award.

Received August 8, 1977.