Elevated irCRH levels up to 14 ng/ml were measured in 176 females in the last trimester. The highest maternal CRH levels were found in those females in whom the period from the onset of labour to full dilatation of the cervix and the time span of delivery were shortest. irCRH in amniotic fluid (120 +/- 180 pg/ml; n = 14) was in the same range as in umbilical cord plasma (233 +/- 188 pg/ml; n = 66) and 20-fold lower than in prepartal maternal plasma (5.38 +/- 4.49 ng/ml; n = 66). irCRH in maternal plasma correlated highly to irCRH in umbilical cord plasma (p less than 0.001; n = 66). After delivery irCRH disappeared from maternal plasma with a half-life of 50 minutes (n = 14). One day postpartum irCRH levels (n = 22) were undetectable. The height of the irCRH levels in the various biological fluids did not correlate to the mode or the pathological events of delivery (n = 43). Maternal ACTH levels above the normal range were encountered only in women immediately prepartal and did not correlate to the CRH levels (253 +/- 229 pg/ml; n = 66). Cortisol levels were higher in maternal plasma than in umbilical cord plasma due to elevated CBG (n = 78). Free cortisol levels were higher in the 3rd trimester than in the 1st (2.18 +/- 0.16 vs 1.16 +/- 0.73 ng/ml; n = 42). irCRH in maternal and umbilical cord plasma correlated to the hPl and estriol levels (p less than 0.001 and p less than 0.05; n = 66). We conclude that irCRH is secreted by the placenta into both maternal and fetal circulation. Though placental CRH is undistinguishable from hypothalamic CRH, the biological significance of placental CRH remains open. Our data show that placental CRH might be responsible for the changed function of the adrenal gland during pregnancy, with higher free cortisol levels in the last trimester. The extremely elevated ACTH levels during labour and delivery indicate that CRH is not the only mediator of stress-induced ACTH secretion in the regulation of the maternal hypothalamo-pituitary-adrenal axis.

No abstract

ACTH secretion was studied in response to repetitive and continuous administration of human corticotropin releasing factor (CRF) in 14 healthy volunteers and 2 patients with secondary adrenal insufficiency. ACTH increases during repetitive CRF administration were within the same range in normal subjects independent of the intervals (60\p=n-\180 min) between the CRF pulses (100 \ g=m\ giv). When CRF was infused continuously (100 \g=m\g/h for 3 h) after an initial CRF bolus injection (100 \g=m\giv), ACTH and cortisol remained elevated during the infusion at a nearly constant level (ACTH: 60 \m=+-\5 pg/ml; cortisol: 21.2 \m=+-\1 \g=m\g/dl ; \l =x_\\ m=+-\SE).A second CRF bolus injection at the end of the infusion did not lead to a significant further increase of ACTH and cortisol levels. This shows that there is no desensitisation or depletion of a ready releasable pool, as it is observed with other pituitary hormones after releasing hormone stimulation. Pulsatile administration of CRF in 2 patients with secondary adrenal insufficiency due to previous cortisol or glucocorticoid excess, respectively, revealed a blunted response to the first pulse which became normal after the following pulses. The latter could not be sustained until the next morning without CRF given overnight. These findings point to a hypothalamic defect being the cause of hypocortisolism after long-term cortisol suppression.Continuous and repetitive stimulation with gona¬ dotropin releasing hormone leads to blunted gonadotropin responses in men due to pituitary

No abstract

No abstract