Maternal plasma corticotrophin-releasing hormone--elevated in preterm labour but unaffected by indomethacin or nylidrin.

The role of corticotrophin-releasing hormone (CRH) in preterm labour was studied in 23 women in preterm labour at between 26 and 33 weeks gestation who were randomly allocated to receive treatment with indomethacin (n = 11) or with nylidrin a beta-sympathomimetic agent (n = 12). Maternal plasma CRH in the preterm group (median 70, range 9-597 pmol/l) before therapy was higher (P less than 0.05) than that in 23 control pregnancies, without uterine contractions, matched for gestational age (median 51, range 4-127 pmol/l). CHR levels determined after 3 and 24 h of treatment showed a 10% decrease in the indomethacin group and 10-20% decrease in the nylidrin group, but these changes were not statistically significant. After cessation of uterine contractions during tocolysis, 12 women proceeded to give birth preterm (less than 37 weeks) and their pretreatment CRH levels (median 195, range 9-597 pmol/l) were higher (P less than 0.05) than those in women whose pregnancy proceeded to term (median 52, range 16-207 pmol/l). In another group of women, full-term labour was not accompanied by any changes in maternal CRH levels. Umbilical plasma CRH levels were 1.1-9.8% of the paired maternal levels and did not rise with advancing gestational age. Nor had the type of delivery (elective caesarean section before labour, or preterm or term vaginal delivery) any effect on fetal CRH levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Corticotropin-releasing hormone in maternal and cord plasma in pre-eclampsia.

The concentration of corticotropin-releasing hormone (CRH) in maternal plasma increases greatly during the last trimester of normal pregnancy. This CRH has been proposed to originate from the placenta. We studied plasma immunoreactive CRH in 46 uncomplicated pregnancies, in 10 pregnant women with chronic hypertension, in 17 women with pregnancy-induced hypertension (PIH) and in 24 women with pre-eclampsia, and correlated it to the levels of corticotropin (ACTH) and cortisol. CRH levels were greatly increased in women with pre-eclampsia, less significantly in women with PIH, while no change was found in pregnant women with chronic hypertension. ACTH levels also were increased in pregnancies with pre-eclampsia or PIH and there was a positive correlation between CRH and ACTH levels. CRH levels in cord venous plasma were significantly increased in pregnancies with pre-eclampsia but cortisol did not show any significant increase. These findings suggest that placental release of CRH into the maternal and fetal circulation is increased in pre-eclampsia.

Response of plasma endorphins, corticotropin, cortisol, and luteinizing hormone in the corticotropin-releasing hormone stimulation test in eumenorrheic and amenorrheic athletes.

We compared pituitary response in the corticotropin-releasing hormone (CRH) test between 9 eumenorrheic and 10 amenorrheic endurance athletes. The maximal oxygen capacity (VO2max), determined using an exercise test on a bicycle ergometer, was larger in amenorrheic (62.7 +/- 1.0 SE mL/min per kg) than in eumenorrheic (54.7 +/- 2.3 mL/min per kg) athletes. A 100 micrograms bolus of human CRH was administered intravenously, and blood samples were collected at -15, 0, 30, 60, 90, and 120 minutes. The mean basal concentrations of endorphins, adrenocorticotropic hormone (ACTH), and cortisol did not show significant differences between the groups. The cumulative response of ACTH in the CRH test was larger in eumenorrheic (7.7 +/- 1.3 pmol/L) than in amenorrheic (3.6 +/- 0.6 pmol/L) athletes, but the response of endorphins and cortisol did not differ between the groups. A negative correlation was found between the VO2max and the ACTH response during the CRH test in the total group of athletes. These findings indicated changes in the function of hypothalamic-pituitary-adrenal axis in amenorrheic athletes that can be attributed to intensive training.

Binding of corticotropin-releasing hormone (CRH) in maternal and fetal plasma and in amniotic fluid.

Placenta secretes corticotropin-releasing hormone (CRH) into the maternal and fetal circulation, but a CRH binding protein in plasma may decrease its biological activity. Using a charcoal adsorption method we found that 92% of added 125I-Tyr-CRH was bound to a binding protein in the nonpregnant plasma, 72% in the plasma at term pregnancy, 90% in umbilical cord plasma, 82% in the amniotic fluid in the second and 25% in the third trimester. CRH added to plasma inhibited the binding of 125I-Tyr-CRH over the concentration range of 0.1-8.8 nmol/l in plasma and of 0.1-2.2 nmol/l in amniotic fluid. There was a significant negative correlation (R = -0.80) between the binding capacity of the CRH-binding protein and CRH concentration in maternal plasma. Plasma or amniotic fluid was incubated with 125I-Tyr-CRH and subjected to gel filtration on Sephadex G-50. The bound radioactivity was eluted at the region of Mr 25-40 kDa and the unbound radioactivity at the location of synthetic CRH. Bound and unbound CRH concentrations were determined using charcoal adsorption method and gel filtration on Sephadex G-50 in ten maternal plasma samples at the third trimester of pregnancy. Following mean percentages were found to be bound: charcoal method 61.9 +/- 6.80% (SE) and gel filtration 62.8 +/- 6.33%. We conclude that the bulk of CRH is bound to a binding protein in maternal and fetoplacental circulation, whereas at term pregnancy the role of the binding is small in amniotic fluid.

Response of plasma beta-endorphin and insulin to oral glucose tolerance test in non-obese women with polycystic ovaries.

Increased responses of plasma insulin and endorphins to the oral glucose tolerance test (oGTT) have earlier been found in obese women. We studied responses of immunoreactive beta-endorphin (ir beta-E) and insulin in plasma to the oGTT in 8 non-obese women with polycystic ovaries (PCO) and in 10 healthy women. An additional control group consisted of 5 healthy women who were fasting during the study period. In the PCO group the insulin and glucose responses to the oGTT were increased, and an increase of ir beta-E from 5.9 +/- 1.5 to 8.6 +/- 2.8 pmol/l was found during the 1st half-hour period of the oGTT. In contrast, no significant change was found during the oGTT in healthy women (3.2 +/- 0.5 and 2.7 +/- 0.65 pmol/l, respectively), and in the fasting control women the mean ir beta-E level (+/- SE) decreased, from 4.5 +/- 1.2 to 3.6 +/- 1.1 pmol/l. These findings revealed increased responses of both plasma ir beta-E and insulin to the oGTT in non-obese women with PCO but their possible causal relationship remained unsolved.