The influence of estrogen and prolactin on Hageman factor (factor XII)
titer in ovariectomized and hypophysectomized rats
EM Gordon, JG Douglas, OD Ratnoff and BM Arafah
The synthesis of prothrombin in hepatic microsomes is augmented in intact
estrogen-treated rats and in hypophysectomized rats treated with purified
prolactin. We investigated the influence of these gonadal and pituitary
hormones on the titer of Hageman factor (factor XII), reportedly elevated
in women using oral contraceptives. Rats were ovariectomized to minimize
the influence of endogenous estrogen and progesterone on the Hageman factor
titer. The administration of progesterone did not alter the plasma
concentration of Hageman factor. In contrast, the infusion of 17
beta-estradiol induced a marked elevation of the plasma Hageman factor
titer, as measured functionally and immunologically. The titer of Hageman
factor was directly related to both plasma estradiol and prolactin
concentrations, indicating that prolactin may play a role in the regulation
of plasma Hageman factor titers. In agreement with this, hypophysectomy
induced a marked decrease in the Hageman factor level. In hypophysectomized
ovariectomized animals, the administration of estradiol restored the
Hageman factor titer to normal levels, whereas the infusion of prolactin
induced a dramatic rise in the Hageman factor titer to the degree observed
in nonhypophysectomized estrogen-treated rats. No further increase in the
Hageman factor titer was observed in rats treated with both estradiol and
prolactin. These data indicate that estrogens increase the plasma Hageman
factor titer both directly and through its release of prolactin and that
prolactin may also increase the titer of Hageman factor through
estrogen-independent mechanisms.
Volume 66,
Issue 3,
pp. 602-605,
09/01/1985
Copyright © 1985 by The American Society of Hematology
