Stimulated LH Release Research Articles

Estradiol and the neuroendocrine control of LH release in vitro.

Release of LH was measured following short-term incubation of rat anterior pituitary (AP) and stalk median eminence (SME) tissue in the presence or absence of estradiol (E2). LH release from AP's incubated alone was enhancedby 0.5 or 1.0 ng E2/ml. This positive effect was blocked by puromycin (10.0 or20.0 μg/ml) or by cycloheximide (10.0 μg/ml), although the antibiotics failed to influence basal release of LH from the incubated glands. LH release in the presence of LRF was not significantly altered by adding E2 in small or high doses (0.5, 1.0 or 25 μg/ml). When AP's were incubated together with SME tissue (2 SME/gland), LH release was not altered by adding 0.5 or 1.0 jug E2/ml to the medium. Dopamine (DA) at a dose of 2.5 μg/ml had been shown earlier to stimulate LH release from the co-incubate via discharge of LH-releasing factor (LRF) from the hypothalamic tissue. Doses ranging from 0.2 to 12.5 μg Ea/ml prevented the responsiveness of the SME to DA; this inhibitory effect of E2 was again blocked by pur...

Stimulation of LH release in men and women by LH-releasing hormone purified from porcine hypothalami.

ABSTRACT LH-releasing hormone (LRH2), purified from porcine hypothalamic tissue, was tested in the human being. The LRH was injected iv into the following 8 subjects: 2 untreated men, 2 untreated women, 2 men pretreated with ethinyl estradiol, and 2 women pretreated with an oral contraceptive preparation (Lyndiol). The design was that of a 4-factor partially nested factorial experiment in which serum LH and FSH levels were measured by specific radioimmunoassays and compared with the values obtained after injection of a control solution of lysine vasopressin. The data indicated a highly significant increase (p <0.01) in serum LH at 23.5 min and a significant increase (p <0.05) in serum FSH at 24.5 min after administration of LRH. There was a 3.7-fold mean increase in serum LH levels with a range of 1.9–7.5, and a 2.2-fold mean increase in serum FSH levels (1.2–4.8). The response to LRH was not significantly influenced by either the sex of the subject or pretreatment with a steroid suppressing LH release. T...

THE CENTRAL NERVOUS SYSTEM, ESTROGEN AND PUBERTY

Median eminence (ME) implants of estradiol performed in 26-day-old female rats induce: a) a precocious opening of the vaginal membrane; b) ovulation, as indicated by the presence of corpora lutea; c) a reduction of pituitary LH stores; d) a concomitant increase of plasma LH levels; and e) an increase in uterine weight. These data suggest that estradiol, when implanted in the ME region of immature female rats, may stimulate LH release through a “positive” feedback effect exerted on specific neural receptors. Implants of estradiol performed in the habenular region (HR) of 26-day-old female rats are followed by: a) retardation of puberty; b) reduction of the weights of the ovaries and of the uteri; c) increase of LH stores in the pituitary. LH remains undetectable in the general circulation, however. It is suggested that the HR contains receptors which are sensitive to the “negative” feedback effect of estrogen and which intervene in the control of LH sectetion. (Endocrinology 83: 1101, 1968)

The central nervous system, estrogen and puberty.

Median eminence (ME) implants of estradiol performed in 26-day-old female rats induce: a) a precocious opening of the vaginal membrane; b) ovulation, as indicated by the presence of corpora lutea; c) a reduction of pituitary LH stores; d) a concomitant increase of plasma LH levels; and e) an increase in uterine weight. These data suggest that estradiol, when implanted in the ME region of immature female rats, may stimulate LH release through a “positive” feedback effect exerted on specific neural receptors. Implants of estradiol performed in the habenular region (HR) of 26-day-old female rats are followed by: a) retardation of puberty; b) reduction of the weights of the ovaries and of the uteri; c) increase of LH stores in the pituitary. LH remains undetectable in the general circulation, however. It is suggested that the HR contains receptors which are sensitive to the “negative” feedback effect of estrogen and which intervene in the control of LH sectetion. (Endocrinology 83: 1101, 1968)

LH release by 17-beta-estradiol in the rat.

A decrease in pituitary LH with a concomitant increase in plasma LH was observed in adult intact female rats injected subcutaneously with 17β-estradiol (0.6 μg/kg) for 7 days. This observation indicates that estradiol is capable of stimulating LH release when administered in a relatively small dose. An estrogen antagonist (CN-55,945-27), which is mildly estrogenic, had no significant effect in preventing the decrease in pituitary LH caused by estradiol treatment. However, the compound (25 μg/kg, orally) did prevent the increase in plasma LH observed with estradiol. This effect was probably due to an additive action between estradiol and CN-55, 945-27 to produce the negative feedback effect of estrogen on LH secretion. Thus, relatively low doses of estrogen are capable of stimulating the release of LH, whereas higher doses inhibit LH secretion. (Endocrinology 79: 455, 1966)

Activation of the adenohypophysis by intravenous injections of epinephrine in the atropinized rabbit.

introduction Markee, Sawyer and Hollinshead (1948) stimulated the release of luteinizing hormone (or total gonadotrophin) from the rabbit hypophysis by the intrahypophyseal injection of small amounts of epinephrine (Adrenalin). After receiving 4 injections of 0.05 ml. epinephrine 1 mg./ml.), 5 out of 10 rabbits ovulated. However, intravenous and intracarotid injections of much higher dosages, up to the MLD, led to completely negative results (op. cit., and Marshall and Verney, 1936). These findings suggested that a discrete adrenergic mechanism, localized in the region of the hypophysis, might control pituitary activation. The presence of such an adrenergic mechanism in the reflex by which coitus stimulates LH release in the rabbit was affirmed by blocking copulation-induced ovulation with the adrenergic blocking agent Dibenamine (Sawyer, Markee and Hollinshead, 1947). Subsequent work revealed that the pituitary activation reflex also contains an atropine-blocked component which apparently precedes the Di...

Evidence that copper acetate induces ovulation in the rabbit by direct stimulation of the adenohypophysis.

Copper salts induce ovulation in the estrous rabbit, a species which normally ovulates only after copulation. The natural mating stimulus, which results in the release of luteinizing hormone from the adenohypophysis, involves the hypothalamus and the pituitary stalk and includes both adrenergic and cholinergic components. Bischoff suggested that copper activated the hypophysis by toxic stimulatory effects on the nervous system. The idea appeared to be confirmed by the results of Brooks, who found that copper failed to induce ovulation in rabbits whose hypophyseal stalks had been severed, and Harris, who reported that very weak dosages of copper acetate injected directly into the third ventricle stimulated the ovulatory response. We were led to doubt that copper-induced ovulation is purely a nerve-stimulation phenomenon when dibenamine and atropine, in dosages adequate to block the copulation stimulus from reaching the hypophysis,, failed to prevent copper acetate from activating the release of an ovulatory surge of LH. It therefore seemed desirable to test the hypothesis that copper might exert its stimulatory action directly upon the anterior pituitary. Sexually mature female rabbits ranging in weight from 2.5 to 4.3 kg were employed; in this study. To insure an estrous condition, each animal was treated with 85 μg estradiol benzoate on 2 successive days prior to copper administration, for ovulation is not induced by copper in anestrous rabbits. A control series of 10 females revealed that the estrogen alone would not stimulate LH release. The hypophysis was approached parapharyngeally as in earlier studies, and 4 attempts were made at 5 or 10s minute intervals to inject a total of 0.15 ml of 0.1% copper acetate, buffered with 0.1% sodium acetate, directly into the pars distalis.