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United States Department of Agriculture

Agricultural Research Service


item Willard, S
item Lay, Jr, Donald - Don
item Friend, T
item Neuendorff, D
item Randel, R

Submitted to: Theriogenology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/21/2004
Publication Date: 2/16/2005
Citation: Willard, S.T., Lay, Jr., D.C., Friend, T.H., Neuendorff, D.A., Randel, R.D. 2005. Plasma progesterone response following ACTH administration in the pregnnant Brahman heifer. Theriogenology. 63:1061-1069.

Interpretive Summary: The role of the adrenal gland and its potential contribution to reproductive function in mammals has been theorized for some time with definitive roles of the fetal adrenal gland and cortisol linked to the initiation of parturition. Further findings of the adrenal gland as a significant source of progesterone in rats, deer, ewes and cows have furthered speculation that the adrenal gland may serve as a supplemental source of progesterone in support of some aspects of reproduction. The actions of supplemental placental and/or fetal adrenal progesterone production have been shown to be supportive of pregnancy by suppressing the maternal immune system to prevent rejection of the developing fetus and placenta, as well as in ensuring myometrial quiescence for the maintenance of pregnancy. In the present study, mid-gestation pregnant Brahman heifers were treated with one of four doses of ACTH and serum concentrations of progesterone determined at various sampling intervals post-challenge. Additionally, the relationship between circulating concentrations of cortisol relative to progesterone was also examined. Collectively, these data indicate that ACTH administration can acutely increase plasma progesterone production above that of normal circulating concentrations in the mid-gestation pregnant Brahman heifer. These increases in progesterone are most likely of adrenal origin, although extra-adrenal sources cannot be ruled out completely. Whether the maternal adrenal gland in some species, including the bovine, plays an active role in the maintenance of pregnancy during periods of acute stress, or when luteal or placental progesterone production becomes compromised, remains to be determined. Findings of this research are useful to researchers to progress in stress physiology research and its relation to reproduction.

Technical Abstract: Previous reports of adrenal progesterone (P4) contributions during late gestation in cattle, and ACTH-induced P4 responses in the non-pregnant heifer, prompted an investigation to evaluate the plasma P4 response and the relative ratio of plasma cortisol (CT) to P4 following ACTH administration in mid-gestation pregnant Brahman heifers. Twenty-three pregnant (139.0 ± 5.0 d of gestation) Brahman heifers received one of the following treatments: 0 (saline; n = 5), 0.125 (n = 4), 0.25 (n = 5), 0.5 (n = 4) or 1.0 (n = 5) IU of ACTH per kg BW. Blood samples were collected at -15 and -0.5 (Time 0), 15, 30, 45, 60, 75, 105, 135, 165, 195 and 255 min post-ACTH challenge. Plasma P4 and CT were quantified by RIA. Pre-ACTH P4 did not differ (P > 0.10) among ACTH treatment groups (pooled: 12.1 ± 0.6 ng/ml). Among peak P4 values at 15 min post-ACTH infusion, control P4 (9.6 ± 1.2 ng/ml) tended to be lower (P < 0.07) than 0.5 IU ACTH-treated heifers (13.3 ± 1.1 ng/ml); and were lower (P < 0.02) than 0.25 and 1.0 IU ACTH-treated heifers (14.7 ± 1.1 and 22.2 ± 3.7 ng/ml, respectively). During the primary P4 response period (0 to 75 min post-ACTH), the area under the curve (AUC) was greater (P < 0.05) for 1.0 IU ACTH-treated heifers than all other groups. The CT: P4 ratios were lower (Time x Treatment, P < 0.01) for control heifers than all ACTH-treated heifers. Among ACTH-treated heifers, CT : P4 ratio response and CT: P4 ratio AUC were similar (P > 0.10) following ACTH challenge. These data suggest that acute increases in ACTH elevate plasma P4, likely of adrenal origin, in mid-gestation pregnant heifers, while the CT : P4 ratio (relative output) remains constant irrespective of ACTH dose (0.125 to 1.0 IU).

Last Modified: 06/26/2017
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