Plasma Prolactin Release Research Articles

Fetal and adult hemoglobin in the chronically catheterized sheep fetus.

The switch from fetal to adult hemoglobin (Hb) has been investigated in fetal and newborn lambs. In the period between 125 and 145 days gestation, the proportion of fetal cells containing adult Hb increased significantly in catheterized fetuses. This increase paralleled the rise in fetal plasma cortisol under several different experimental conditions. However, infusion of synthetic adrenocorticotropin (ACTH1-24) into the fetus, which increased fetal plasma cortisol concentrations to levels slightly higher than observed at term, did not bring about any increase in the proportion of cells containing adult Hb. Increasing fetal plasma prolactin (PRL) concentration either by infusion of PRL or by stimulating endogenous PRL release with thyrotropin-releasing hormone (TRH) did not influence the time or rate of the switch. The fetal reticulocyte count was significantly higher in blood samples taken at the time of catheterization in fetuses of 103-115 days gestation than at 116-128 days gestation. In one repeatedly sampled fetus of adult type Hb AB, Hb C was observed at the time when the fetus was anemic. At birth the number of cells containing adult Hb was significantly higher in catheterized lambs than in nonoperated controls.

Inhibition of naloxone of prolactin release induced by L-5-hydroxytryptophan in rats.

AbstractIntravenous injection of l-5-hydroxytryptophan (l-5-HTP), but not l-5-HTP, resulted in an increase in plasma prolactin (PRL) levels in anesthetized rats. l-5-HTP-induced PRL release was blunted by naloxone, a specific opiate antagonist. In rats pretreated with either reserpine or α-methyl-p-tyrosine (α-MT), basal plasma PRL levels were elevated and l-5-HTP injection caused a further increase in plasma PRL concentrations. However, PRL release induced by l-5-HTP was not blunted by naloxone in these animals pretreated with reserpine and α-MT. These results suggest that PRL release induced by serotonin is modulated, at least in part, by opioid peptidergic mechanisms, which are closely related to brain catecholamines.

Role of Prolactin in the Polycystic Ovary Syndrome

Studies with a dopamine agonist (Bromocriptine) and an antagonist (Haloperidol) suggest that elevated sex steroid synthesis such as may be found in the polycystic ovary syndrome (PCO) influence the pituitary lactotrope response to endogenous control mechanisms. A distinction between PCO with occasional elevation of plasma prolactin (PRL) and the galactorrhoea-amenorrhoea syndrome (GA) associated with hyperprolactinaemia can be established on the basis of differences in circulating levels of sex steroids and in the pattern of response to lactotrope cell stimulation. Thus, adrenal androgen synthesis can be strengthened in GA whereas in PCO both pathways, adrenal and ovarian, may be overstimulated. Also blunted PRL response to TRH or dopaminergic blockade is often seen in GA. The use of bromocriptine in patients with PCO and elevated PRL plasma levels has been shown to restore ovulation. The possible implications of dopaminergic mechanisms in the control of LH secretion independent of PRL release are discussed.

Effect of Calcitonin on prolactin release in rats

Injection of [Asu 1,7]-eel calcitonin (CT) (0.1–2.5μg) into the lateral ventricle resulted in a significant and dose-related increase of plasma prolactin (PRL) levels in urethane-anesthetized male rats. Naloxone failed to block [Asu 1,7]-eel CT induced PRL release. Salmon CT, human CT and porcine CT were similarly effective to stimulate PRL release when injected intraventricularly. Intravenous administration of [Asu 1,7]-eel CT(20 μg) failed to cause any significant changes in plasma PRL levels, while this peptide (10 −8−10 −6M) possesed a mild stimulating activity of PRL release from the anterior pituitary cells cultured in vitro . These results suggest that CT stimulates rat PRL secretion mainly through the central nervous system like one of the neurotransmitters, though it may also act directly on the pituitary.

Prolactin-Lowering Effect of Nomifensine in the Rat

The effect of nomifensine (Nom), a new antidepressant agent which facilitates dopaminergic neurotransmission by blocking the reuptake of dopamine (DA) into nerve terminals and by promoting DA release, was studied on plasma prolactin (PRL) levels in the rat. Nom reduced baseline plasma PRL levels in untreated or reserpine-pretreated male rats and in ovariectomized, estrogen-primed female rats. Nom did not alter plasma PRL levels in reserpine-α-methyl-p-tyrosine-pretreated male rats and in hypophysectomized female rats bearing a pituitary transplant under the kidney capsule nor inhibited PRL release from in vitro-in-cubated pituitaries. The availability of drugs such as Nom, whose action rests on the integrity of dopaminergic transmission in the CNS, without involving direct stimulation of pituitary DA receptors, offers a valid means to investigate CNS function in hyperprolac-tinemic states.

Mechanism of Reversible Loss of Reproductive Capacity in a Seasonally‐Breeding Mammal

Reversible loss of fertility which occurs annually in seasonally‐breeding species appears due to changes in the release of pituitary hormones, the levels of gonadal hormone receptors and the sensitivity of the hypothalamic‐pituitary system to inhibition by gonadal steroids. In the golden hamster, exposure to a short photoperiod causes reduction in plasma prolactin (PRL) levels, loss of testicular LH receptors, and gonadal atrophy. Reduction in plasma PRL is probably not secondary to inhibition of testicular steroidogenesis because it cannot be induced by castration or reversed by administration of testosterone. Treatment of gonadally regressed hamsters with PRL increases testicular weight, spermatogenesis, concentration of LH receptors in the testis and plasma testosterone levels. Prolactin‐producing ectopic pituitary homografts prevent loss of LH receptors and delay gonadal regression in animals transferred from a long to a short photoperiod. Treatment of adult male hamsters with PRL can increase plasma FSH levels. It is concluded that changes in PRL release play an important role in mediating the effects of photoperiod on testicular activity in the golden hamster.

Action of metergoline in suppressing prolactin release induced by mechanical breast emptying.

Ten women were studied during the first post-partum week. Mechanical breast emptying with a breast pump for 30 min induced a marked increase in plasma prolactin (PRL) reaching a maximum 30 min after the beginning of stimulation. In all patients oral administration of the antiserotonin agent metergoline, 8 mg daily for two days, completely blocked any PRL secretion induced by breast stimulation. These results confirm the inhibitory effect of metergoline on PRL release.

Plasma prolactin in undisturbed cannulated male rats; effects of perphenazine, frequent sampling, stress and castration plus oestrone treatment.

ABSTRACT Blood was collected from undisturbed male rats by means of chronically indwelling intrajugular cannulae and the plasma prolactin (PRL) concentration was determined by a radioimmunoassay. The effect of perphenazine, frequent bleeding, handling and brief ether stress in normal males and of stress in castrated oestrone treated males was determined. The plasma PRL concentration in undisturbed intact males was low. Castration plus oestrone treatment for 3 or 7 weeks had little or no effect on the PRL concentration. Neither frequent blood sampling nor removal of 3 ml blood over a period of 5 h affected plasma PRL concentration. Intravenous administration of perphenazine caused a striking and prolonged increase in plasma PRL in intact males. Brief handling or mild ether stress caused a significant rise in PRL within 2 min in intact males; 15–20 min later PRL had returned to the undisturbed level. Brief ether stress in oestrone treated castrates induced a comparable pattern of prolactin release, although of greater magnitude. In these animals a second stress one hour later induced a similar response. It is concluded that chronic cannulation neither affects the unstressed prolactin level nor interferes with the ability of the adenohypophysis to release PRL. The results also indicate that when rats are handled a truly stress free sample can only be obtained when the blood is drawn within one minute after the initial disturbance of the animal. The evidence presented indicates that oestrone treatment increases the responsiveness of male rats to stress-induced PRL release.

Plasma prolactin release about oestrus and after suckling in the beef cow.

Plasma prolactin release about oestrus and after suckling in the beef cow.