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Adrenocorticotropin and Cortisol Responses to Vasopressin during Pregnancy^*

Departments of Medicine, Obstetrics and Gynecology and Pediatrics, Columbia University College of Physicians and Surgeons New York, New York 10032

Address all correspondence and requests for reprints to: Dr. Robin S. Goland, Department of Medicine, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, New York 10032.

CRH is secreted by the placenta into the maternal and fetal circulation during pregnancy in humans and nonhuman primates. ACTH and cortisol responses to exogenous CRH are blunted during pregnancy. In the present study we examined the pituitary-adrenal response to another corticotropin releasing factor, vasopressin. Studies were performed in chronically catheterized female baboons moving freely in their home cages; 13 studies were performed in 4 pregnant animals, and 8 studies were performed in 6 nonpregnant animals. Vasopressin was administered iv in 2 doses (0.3 and 3.0 U), and plasma samples were obtained for CRH, ACTH, and cortisol measurements. Results are expressed as the mean ± SEM. Baseline plasma CRH was 240 ± 20 pmol/L in the pregnant animals and unmeasurable (<20) in the nonpregnant animals. In the pregnant animals, ACTH concentrations rose from a baseline of 6.4 ± 1.3 pmol/L to 10.1 ± 0.4 after 0.3 U vasopressin and to 24.9 ± 5.2 after 3.0 U vasopressin. In the nonpregnant animals, ACTH levels were 5.8 ± 1.3 at baseline, 6.7 ± 1.3 after the 0.3-U dose, and 14.6 ± 2.4 after the 3.0-U dose. The peak ACTH response after each dose of vasopressin was higher in the pregnant animals than in the nonpregnant animals (P < 0.05). The baseline cortisol level in the pregnant animals was 960 ± 80 nmol/L and rose to 1370 ± 110 and 1535 ± 165 after the 2 doses of vasopressin, respectively. The baseline cortisol concentration in the nonpregnant animals was 910 ± 86 nmol/L. The cortisol level was 990 ± 75 after the 0.3-U vasopressin dose and 1380 ± 140 after the 3.0-U dose. The peak cortisol response after the 0.3-U dose was significantly higher in the pregnant animals (P < 0.02), while the peak cortisol responses after the 3.0-U dose were similar in the 2 groups of animals. In a single animal, vasopressin was administered sequentially at 4 gestational ages during pregnancy and then 2 times in the postpartum period. The ACTH response to vasopressin increased as pregnancy progressed and then decreased in the postpartum period. In summary, the ACTH and cortisol responses to 0.3 and 3.0 U vasopressin, iv, are enhanced during pregnancy in the baboon, although the responses to exogenous CRH are blunted during gestation. We conclude that the chronic placental CRH stimulation of the pituitary-adrenal axis during pregnancy leads to an enhanced response to vasopressin and a down-regulation of the response to exogenous CRH.

^* Presented in part at the 72nd Annual Meeting of The Endocrine Society, Atlanta, GA, June 20–22, 1990. This work was supported by USPHS Grants HD-13036 and HD-00821.

¹Goland, R. S., I. M. Conwell, W. B. Warren, and S. L. Wardlaw, submitted.

Received November 28, 1990.

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