Diurnal variations and temporal coupling in the circulating levels of immunoactive and bioactive luteinizing hormone (LH) and prolactin (PRL), testosterone (T) and 17-beta-estradiol (E2) in plasma of 6 healthy men (mean age 33 years) were studied. Each hormonal profile was analyzed for circadian amplitude, acrophase and nadir. Acrophases for immunoactive LH and T were coincident and ranged between clock hours 1 and 5. Acrophase for bioactive LH ranged between 9 and 12 h and was coincident with nadir for T. Acrophase for E2 ranged between 15 and 18 h and was coincident with nadir for immunoactive LH (15–17 h). Acrophase for bioactive PRL and immunoactive PRL ranged between 20–23 and 23–4 h, respectively. The circadian amplitude for T showed a negative correlation coefficient with circadian amplitude of bioactive LH (alpha = -0.86) and positive correlation coefficient with circadian amplitude of immunoactive LH (alpha = 0.94). It is inferred that immunoactive LH may be a sensor of T concentration while bioactive LH may be actually involved in the feedback regulation of T secretion. It is suggested that PRL may have a key role in the regulation of LH secretion.
We have recently demonstrated that the pituitary hypothalamic complex (PHC) is a good model for studying interactions between the hypothalamus and pituitary in vitro. The amount of prolactin secreted by the PHC is an index of prolactin secreted by the pituitary in the presence of hypothalamic control, while the amount released by the whole pituitary alone is an index of prolactin secreted in the absence of hypothalamic control. The amount of prolactin secreted by the PHC has been regarded as an index of hypothalamic prolactin-releasing activity (HPRA), while the difference in the amounts of prolactin secreted by the whole pituitary and the PHC is the hypothalamic prolactin-inhibiting activity (HPIA). Attempts were made to correlate HPRA and HPIA to the development of serum concentrations of prolactin from days 7 to 77 in male rats. The HPRA increased steadily from days 7 to 56, decreased significantly on day 63 and thereafter remained unchanged until day 77. The HPIA was low on days 7 and 14 and increased steadily up to day 49, with no further significant variations. The developmental patterns of HPRA and HPIA were comparable up to day 49. Serum concentrations of prolactin increased significantly until day 28 and remained fairly constant until day 49. The weight of the pituitary gland increased from 1.0 +/- 0.03 mg (mean +/- S.E.M.) on day 7 to 7.76 +/- 0.32 mg on day 63 and remained unchanged thereafter. The weight of the hypothalamic islet was 31.5 +/- 2.88 mg on day 7, 34.83 +/- 1.45 mg on day 14 and 50.4 +/- 4.01 mg on day 21. After day 21 the weights of the hypothalamic islets were not significantly altered, except on day 49. It was concluded that serum concentrations of prolactin are regulated by interaction or competition between HPRA and HPIA at the level of the pituitary.
Comparative in vitro studies on the release of LH and FSH by pituitary-hypothalamus complex (PHC) with intact portal plexus and whole pituitary (PI) from adult male rats showed that PHC released LH at a greater rate and in larger amounts than PI. PHC and PI released FSH in comparable amounts and rates. Attempts were made to correlate serum gonadotropin levels to that released by PHC and PI at 1, 3, 7, 14, 21 and 46 days of post-castration (PC). Sham operated animals served as controls. Castration increased serum LH and FSH levels but in different profiles. CPHC and CPI (PHC and PI from castrated rats) released less LH than NPHC and NPI (PHC and PI from sham operated controls) till day 14 PC after which CPHC and CPI released more LH than NPHC and NPI respectively. Castration abolished the intrinsic capacity of PHC to secrete more LH than PI. CPHC and CPI secreted significantly less FSH than NPHC and NPI at 1, 3 and 7 days PC. At days 14 and 21 of post-castration PCNCP or CPI and NPHC or NPI released similar amounts of FSH. Administration of 5 alpha-dihydrotestosterone (DHT, 1 mg/rat/day) or estradiol valerate (EV, 1 microgram/rat/day) immediately following castration prevented the rise in serum LH and FSH but increased the amounts of LH and FSH released by CPHC and CPI. The treatment caused a marked stimulation of FSH released by CPI.(ABSTRACT TRUNCATED AT 250 WORDS)
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