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  • Title: Oxytocin in human plasma: correlation with neurophysin and stimulation with estrogen.
    Author: Amico JA, Seif SM, Robinson AG.
    Journal: J Clin Endocrinol Metab; 1981 May; 52(5):988-93. PubMed ID: 7228998.
    Abstract:
    RIA for the measurement of oxytocin in human plasma is described. Extraction of oxytocin from larger peptides in plasma used acetone precipitation with a 75% +/- 2 SEM recovery of oxytocin. Nonspecific binding of the assay was less than 4%, and the minimum level of detection was 0.2 microunits/tube. No cross-reactivity was noted with neurophysins, arginine, or lysine vasopressin. The mean basal level (+/- SEM) of oxytocin in men was 1.80 +/- 0.07 microunits/ml and was not different in normal women (1.71 +/- 0.07 microunits/ml). Changes in posture had no effect on the levels of oxytocin. Samples obtained every 15 min over 4 h showed no pulsatile secretion of oxytocin. In women chronically receiving estrogen as an oral contraceptive, oxytocin was greater than normal, (4.59 +/- 0.51 microunits/ml; P less than 0.01). Estrogen-stimulated neurophysin was also elevated (8.45 +/- 1.99 ng/ml; P less than 0.005). Acute ingestion of estrogen caused an increase in the level of oxytocin in plasma by 12 h and a concomitant elevation of estrogen-stimulated neurophysin. When the neurophysin was isolated from plasma obtained from a subject after ingestion of estrogen, the neurophysin from plasma comigrated on a polyacrylamide gel with a human pituitary standard of estrogen-stimulated neurophysin. In the studies in which neurophysin was elevated, the correlation between the level of oxytocin and the level of estrogen-stimulated neurophysin in plasma was significant (P less than 0.01). The observation that estrogen administration stimulates the release of oxytocin and estrogen-stimulated neurophysin provides additional evidence that this neurophysin is the oxytocin-neurophysin of man. RIA for the measurement of oxytocin in human plasma is described. Extraction of oxytocin from larger peptides in plasma used acetone precipitation with a 75% +or- 2 SEM recovery of oxytocin. Nonspecific binding of the assay was less than 4% and the minimum level of detection was 0.2 mcU/tube. No cross-reactivity was noted with neurophysins, arginine, or lysine vasopressin. The mean basal level (+or- SEM) of oxytocin in men was 1.80 +or- 0.07 mcU/ml and was not different in normal women (1.71 +or- 0.07 mcU/ml). Changes in posture had no effect on the levels of oxytocin. Samples obtained every 15 minutes over 4 hours showed no pulsatile secretion of oxytocin. In women chronically receiving estrogen as an oral contraceptive, oxytocin was greater than normal (4.59 +or- 0.51 mcU/ml; P0.01). Estrogen-stimulated neurophysin was also elevated *8.45 +or- 1.99 ng/ml; P0.005). Acute ingestion of estrogen caused an increase in the level of oxytocin in plasma by 12 hours and a concomitant elevation of estrogen-stimulated neurophysin. When the neurophysin was isolated from plasma obtained from a subject after ingestion of estrogen, the neurophysin from plasma comigrated on a polyacrylamide gel with a human pituitary standard of estrogen-stimulated neurophsin. In the studies in which neurophysin was elevated, the correlation between the level of oxytocin and the level of estrogen-stimulated neurophysin in plasma was significant (P0.01). The observation that estrogen administration stimulates the release of oxytocin and estrogen-stimulated neurophysin provides additional evidence that this neurophysin is the oxytocin-neurophysin of man.
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