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Endocrinology, doi:10.1210/endo-115-3-1004
Endocrinology Vol. 115, No. 3 1004-1010
Copyright © 1984 by the Endocrine Society.
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Evidence that the Maternal Pituitary Suppresses the Secretion of Relaxin in the Pregnant Rat*

T. G. GOLOS{dagger} and O. D. SHERWOOD

University of Illinois College of Medicine and the Department of Physiology and Biophysics, University of Illinois at Urbana-Champaign Urbana, Illinois 61801

Address requests for reprints to: Dr. O. D. Sherwood, Department of Physiology and Biophysics, 524 Burrill Hall, 407 South Goodwin, University of Illinois, Urbana, Illinois 61801.

Abstract

The role of the pituitary in regulating relaxin synthesis and secretion by the corpus luteum during the second half of pregnancy was investigated by hypophysectomizing rats carrying either one conceptus (1C) or a full complement (FC) of conceptuses (n ≥ 8) on day 13 of pregnancy. Serum and luteal relaxin levels, serum progesterone levels, and luteal weights in 1C rats were markedly lower during the period from days 14 through 20 of pregnancy than those in FC rats, as has been previously reported. After hypophysectomy of 1C rats (HlC), serum relaxin levels, serum progesterone levels, and corpus luteum weights increased to values that were not significantly different from those of FC rats. Additionally, hypophysectomized FC rats (HFC) had higher serum relaxin levels than FC rats. Luteal relaxin content was unaffected by hypophysectomy i n spite of increased relaxin secretion. Other workers have suggested that placental testosterone may support luteal function during the second half of pregnancy. Serum testosterone levels in 1C rats were markedly lower than those in FC rats, but did not increase after hypophysectomy in either HlC or HFC rats. It is concluded that the putuitary has a suppressive effect on relaxin secretion (and perhaps synthesis) as well as progesterone secretion and corpus luteum growth, and that increased luteal function after hypophysectomy is not due to increased placental testosterone secretion. (Endocrinology 115: 1004–1010, 1984)

Footnotes

* This work was supported by NIH Grant USPHS HD-08700.

{dagger} Recipient of Predoctoral Research Service Award 5T32-GM-7283.

Received November 9, 1983.




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