Purification of human prolactin.
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Biomedical subjects
Publications and source records attributed to H Guyda.
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Administration of a single dose of Gondotrophin Releasing Factor (GnRF) failed to induce an increase in serum FSH immediately postpartum suggesting pituitary refractoriness. However, multiple injection of GnRF resulted in significant FSH increments but these were less than the FSH responses to a single injection of GnRF in normal menstruating women.
Morphine administration in man results in a significant increase in serum prolactin without altering the levels of growth hormone, thyroid stimulating hormone and cortisol. Apomorphine prevented the morphine induced prolactin rise. It is suggested that the effect on prolactin is not mediated via non specific stress or changes in the thyroid stimulating hormone releasing factor, but via suppression prolactin inhibiting factor or activation of a specific prolactin releasing factor.
Clonidine (0.15 mg iv), a selective noradrenergic receptor agonist, increased serum growth hormone (GH) levels (greater than 6 ng/ml) on 8 out of 12 administrations to 6 normal men. This increase was independent of the hypotensive effects of the drug and unrelated to changes in serum cortisol. Clonidine induced a hyperglycemic effect in all subjects which was greatest 15 min after commencint the injection. No changes in blood sugar or GH occurred after placebo injection. Apomorphine, a selective dopamine receptor agonist, elevated GH in each of these 6 subjects (greater than 10 ng/ml). Clonidine had no effect on serum prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), or thyroid-stimulating hormone (TSH). These data are compatible with a dual dopaminergic and noradrenergic mechanism modulating GH secretion in normal men and with the absence of a noradrenergic mechanism in the regulation of PRL, LH, FSH, or TSH.
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Stimulation and inhibition tests are proposed for evaluating prolactin secretion. Thyrotropin-releasing hormone (TRH) stimulates the release of prolactin from the pituitary. Chlorpromazine acts presumably at the hypothalamic level to increase prolactin secretion. L-Dopa (D,L-alpha-hydrazino-alpha-methyl-beta-[3,4-di-hydroxyphenyl]) has the opposite effect; it inhibits prolactin secretion and may be effective in suppressing galactorrhea.
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A radioimmunoassay for primate prolactin has been developed, with [(131)I] monkey prolactin, and antibodies to monkey or human prolactin. The assay is specific for prolactin; human growth hormone, and human and monkey placental lactogen show no significant crossreaction. The assay is sensitive enough to measure prolactin concentrations in the sera of most humans studied. The concentration of prolactin in the serum of normal children and adults of either sex was usually below 30 ng/ml, while very high concentrations (up to 500 ng/ml) were observed in newborn infants. The serum prolactin concentration during the menstrual cycle showed no definite increase in the luteal phase. Of 24 patients with galactorrhea, 20 had prolactin concentrations above 30 ng/ml; the highest value observed was 1500 ng/ml. In contrast, 12 of 13 patients with acromegaly had concentrations within the normal range. During pregnancy, the concentration of prolactin in serum rose progressively from an average of 30 ng/ml in the first trimester to 200 ng/ml at term. Postpartum, prolactin concentrations fell to normal levels after 1-2 weeks. Suckling was a potent stimulus to prolactin release, increasing its concentration in serum some 10- to 20-fold.
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