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Response to Corticotropin-Releasing Hormone during Pregnancy in the Baboon^*

Departments of Medicine 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 human maternal and fetal plasma during gestation. In the present study plasma CRH was measured in the plasma of five pregnant baboons and their fetuses to ascertain whether the baboon is a suitable model for study of placental CRH. Studies were performed in chronically catheterized animals that exhibited no behavioral or endocrinological signs of stress; maternal animals moved freely about the cage. Mean maternal plasma CRH was 620 ± 110 pmol/L (2970 pg/mL) at 146 ± 11 days gestation, and mean fetal plasma CRH was 133 ± 29 pmol/L (640 pg/mL) at delivery in four animals. Plasma CRH was undetectable (<8.5 pmol/L; <41 pg/mL) in nonpregnant animals and in animals 8 h after delivery. Maternal and fetal plasma CRH levels in the chronically catheterized baboon were very similar to human maternal and umbilical cord CRH levels at comparable gesta-tional ages. In addition, the majority of maternal plasma CRH eluted in the same position as synthetic human CRH by gel filtration.

CRH stimulation tests were performed in the chronically catheterized maternal baboon to investigate whether pituitary-adrenal function during pregnancy is similar to that observed after chronic CRH infusion; blunted ACTH and cortisol responses to acute injections of CRH are observed after chronic CRH infusion. The administration of 0.5 µg/kg ovine CRH (oCRH) failed to result in an ACTH or cortisol rise in four pregnant baboons. Baseline ACTH levels were 5.2 ± 0.4 pmol/L (23.5 pg/mL), and baseline cortisol levels were 800 ± 55 nmol/L (29.1 µg/dL); neither rose after CRH administration. In contrast, 0.5 µg/kg oCRH did result in significant ACTH and cortisol elevations in five nonpregnant baboons [ACTH: baseline, 5.9 ± 1.4; peak, 16 ± 4.8 pmol/L (P < 0.05); cortisol: baseline, 430 ± 55 nmol/L; peak, 960 ± 200 nmol/L (P < 0.05)]. In contrast, the administration of a larger dose of oCRH (5.0 µg/kg) led to stimulation of ACTH release in five pregnant baboons (baseline, 6.6 ± 1.3 pmol/L; peak, 34.1 ± 6.4; P < 0.001). After this dose cortisol levels also rose in the pregnant animals (baseline = 1040 ± 30 nmol/L; peak, 1620 ± 130); however, this response was blunted compared to that in the nonpregnant animals (P < 0.05). CRH (5.0 µg/kg) significantly stimulated both ACTH and cortisol in the nonpregnant animals. We conclude that similar levels of maternal and fetal plasma CRH concentrations are present in the baboon and the human during pregnancy and that the baboon is an excellent model in which to study the physiology of placental CRH. In addition, our findings of blunted ACTH and cortisol responses to exogenous CRH administration during pregnancy in the baboon support the hypothesis that placental CRH modulates maternal pituitary-adrenal function during pregnancy.

^* Presented in part at the 70th Annual Meeting of The Endocrine Society, New Orleans, LA, June 8–11, 1988. This work was supported by USPHS Grants HD-00821 and HD-13063.

Received August 14, 1989.

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