Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum LH and FSH were measured at 60, 30, and 0 min before, at 5, 15, and 30 min during, and at 10, 45, and 90 min after bilateral electrical stimulation (ES) of various hypothalamic regions in 12 unanesthetized ovariectomized rhesus monkeys. ES of the arcuate-ventromedial nuclei (medial basal hypothalamus; MBH) induced a prompt increase in serum LH that persisted throughout stimulation and returned to basal levels within 90 min thereafter. FSH was also released, but the release was slower and less dramatic than that of LH. Sham stimulation (0muA) caused no change in serum gonadotropins. The amount of LH released after MBH-ES depended upon current strength (1.0 mA greater than 0,5 or 0.7 mA). Three sequential 30-min MBH-ES trials at 90-min intervals induced comparable LH responses and 3 h of continuous MBH-ES maintained elevated serum LH levels throughout the stimulation period, suggesting that these stimulation period, suggesting that these stimulation parameters did not completely deplete pituitary stores of releasable LH. The character of the LH response was similar in individual monkeys through 3 to 24 trials during 4 to 18 months. Comparisons were made of the effects of estradiol-17beta (E2) treatment at different doses and for different intervals of time before MBH-ES. ES-induced LH release was not affected by low levels (25 and 55 pg/ml) ofE2 for 48 h, but was reduced by higher E2 concentrations (100 or 230 pg/ml). E2 concentrations of 100 pg/ml had no effect at 24 h, but reduced MBH-ES-activated LH release at 48 to 96 h; the degree of depression was time-related (48 h less than 72 h less than 96 h). ES of the preoptic-suprachiasmatic region (rostral hypothalamus; RH) in non-E2-treated monkeys also released LH, but this increase was less than after MBH-ES. FSH release was not measurable after RH-ES. In contrast to the depressed LH response to MBH-ES after 48 h of E2 (100 pg/ml), the response to RH-ES was not inhibited by this E2 regimen. These data suggest that ES of an area extending caudally from the rostral hypothalamus to the arcurate-median eminence region will evoke LH release in rhesus monkeys. This electrically induced gonadotropin release was affected by administration of physiological levels of E2 but the nature of effect depended on the specific region stimulated: distinct inhibition of the gonadotropic response to MBH-ES and slight facilitation of the response to RH-ES.
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PMID:Effects of estradiol-17beta on the induction of gonadotropin release by electrical stimulation of the hypothalamus in rhesus monkeys. 1 30

Ram "rete testis" fluid (RTF) routinely collected throughout the year has been used as a source of inhibin. The mean flow rate and mean concentration of spermatozoa in the fluid remained constant during the first 12 days of cannulation. More than 50 castrated or cryptorchid rams have been treated with low doses of steroid-free RTF over a 25-h blood sampling period. Human serum albumin was injected as a control. RTF depressed both FSH and LH plasma levels although the pattern was different for each hormone. There was no change in prolactin secretion. LH secretion was affected first while FSH remained unchanged in castrated and in cryptorchid rams. Thereafter, the maximum depression of FSH plasma levels occurred at a time when LH started to return or had returned to preinjection levels in the cryptorchid and castrated animals respectively. In the cryptorchid rams, RTF suppressed pulsatile LH secretion which was present before treatment but in the castrated animals, RTF lowered LH plasma levels which were constant and showed no pulsatile changes before treatment. Both FSH and LH inhibitory activities have been found in all active fractions obtained by purification of RTF. These activities are papain-sensitive and active fractions have a high apparent molecular weight (greater than or equal to 100 000) as shown by gel filtration and ultrafiltration. These and other results in the literature have lead to a re-definition of inhibin as a protein factor of gonadal origin able to depress plasma levels of FSH and LH, even at low doses.
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PMID:Inhibin activity in ram rete testis fluid: depression of plasma FSH and LH in the castrated and cryptorchid ram. 4 91

The effects of the ergoline derivative, lergotrile mesylate, on the serum levels of PRL, GH, TSH, LH, FSH, cortisol, and blood sugar were studied in six normal males. The effects of lergotrile mesylate on the serum levels of GH and PRL were also studied in eight patients with acromegaly and in two with idiopathic hyperprolactinemia. In the normal subjects, 2 mg oral lergotrile lowered basal PRL levels after 90 min and markedly impaired the PRL response to TRH (200 micrograms iv); the mean peak value +/- SE was 8.3 +/- 1.1 micrograms/liter, compared to the control value of 66.6 /+- 11.3 micrograms/liter. Lergotrile raised serum GH levels in five of the six subjects to peaks of 8-49 micrograms/liter, compared to 2-8 micrograms/liter after placebo. In three subjects, the GH response to lergotrile was attenuated by the prior administration of the dopamine antagonist, metoclopramide (10 mg orally). Lergotrile had no effect on FSH and LH levels under basal conditions or after the gonadotrophin-releasing hormone (GnRH; 100 micrograms iv). Circulating TSH levels were unaltered basally but impaired after TRH. Blood sugar levels were unaltered; serum cortisol was elevated in five of six subjects; there was a brief depression of diastolic blood pressure, but no change in pulse rate. The side effects after lergotrile were variable, with drowsiness as a consistent feature. These actions are similar to those of bromocriptine (an ergot derivative treatment of hyperprolactinemia and acromegaly, to suppress PRL and GH secretion, and in parkinsonism. Therefore, it may be expected that lergotrile could fulfill these clinical uses; however, in the studies comparing the effects of single oral doses of lergotrile (2 mg) and bromocriptine (2.5 mg) on GH and PRL secretion in patients with acromegaly and hyperprolactinemia, lergotrile in the dose used has been found to have an earlier onset and shorter duration of action.
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PMID:Effect of the dopamine agonist, lergotrile mesylate, on circulating anterior pituitary hormones in man. 4 63

15 patients with formerly endogenous recurrent depression or manic-depressive illness free of psychotic symptoms, who are under lithium prophylaxis about 3,9 years, and 16 healthy controls with approximately the same age and sex were tested with 0,1 U Insulin/kg, 200 micrograms TRH and 50 micrograms LHRH for their hGH-, TSH-, hPRL-, FSH-, LH-and Cortisol levels about 2 hours. hPRL, FSH and LH did not show any change under lithium salts. All patients under lithium showed elevated TSH-levels under basal conditions and after stimulation compared with the control groups. For the young women before menopause the difference was highly significant. Men and praemenopausal women had significantly higher hGH-levels after stimulation under lithium than the normal controls. However postmenopausal women did not show this lithium effect on their hGH levels.
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PMID:[Neuroendocrinological changes under longterm therapy with lithium salts (author's transl)]. 11 22

Hormone production in a patient suffering from a late recurrence of a granulosa cell tumour has been studied pre- and post-operatively, and a vein on the tumour surface was cannulated at operation to collect tumour vein blood for pre-operative studies. Elevation in the plasma oestradiol level and depression in FSH and LH were found pre-operatively, and elevations were found in tumour vein oestradiol and 17alpha-hydroxyprogsterone. Plasma oestradiol level returned to normal postoperatively whereas FSH and LH levels were persistently depressed. FSH receptors were found in this tumour, and on the basis of this finding, gonadotrophins were given to athymic nude mice in an attempt to support the growth of the granulosa cell tumour implanted in these animals. We demonstrated that gonadotrophins have supported the tumour tissue, but not promoted growth.
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PMID:Demonstration of an FSH receptor in a functioning granulosa cell tumour. The effect of gonadotrophin treatment on its viability following transplantation to nude mice. 19 50

A synthetic steroid compound derived from testosteron (isoxazol-ethisterone), Danazol, with gonadotropin-depressing activity, was used in the treatment of 4 cases of idiopathis sexual precocity (age 2 1/2 to 4 years) and in 10 cases of severe pubertal gynaecomastia. In sexual precocity the suppression of menstruation as well as of breast-enlargement was good, while the suppression of acceleration of longitudinal growth and bone maturation was inferior compared with cyproteron-acetate. In most boys with gynaecomastia a marked regression of breast enlargement occurred within a few weeks or months. With the dosage used (200-300 mg/day in the sexual precocity patients, 300-400 mg in the gynaecomastia patients) the changes in plasma hormone levels (LH, FSH, progesterone, estradiol, testosterone) were within a non significant range. Depression of testosterone seemed to be a rather regular finding. No untoward side-effects of the medication were noticed in the 14 patients studied. In summary, Danazol did not show any advantages compared with the compounds used in the treatment of isosexual precocity sofar. In contrast, the drug proved to have useful effects in pubertal gynecomastia, a condition which in severe degrees certainly deserves medical treatment.
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PMID:[A new antigonadotropin in the treatment of precocious puberty and pubertal gynaecomastia (author's transl)]. 19 73

Of 300 menopausal patients, 82 experienced climacteric symptoms, with vasomotor disturbances absent in 42 (Group 1) and present in 40(Group 2). Group 2 patients commonly complained of headaches, insomnia and dyspareunia, while Group 1 complained mostly of loss of libido and depression. Group 2 was managed rather successfully with treatment of conjugated equine estrogens (Premarin) daily for 3 weeks; Group 1 was given the same treatment but the response was disappointing. Women with vasomotor symptoms exhibited a lower, mean plasma estradiol concentration compared with that observed during days 1-10 of the menstrual cycle. Concenerations of FSH (Plasma follicle stimulating hormone) and LH (luteinizing hormone) in women with vasomotor symptoms were similar to those of younger, regularly menstruating women. Group 2 patients treated for 6 months with estrogen had a 2.1 fold increase in mean plasma estradiol concentration and 39% and 66% reduction of pretreatment plasma FSH and LH concentrations, respectively; Group 1 did not exhibit such changes. Patients with estrogen-responsive symptoms exhibited high concentrations of FSH (15 U/1 was the diagnostic cut-off point). Effective patient selection for estrogen replacement therapy can be achieved by using this measurement in the presence of characteristic symptoms.
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PMID:Relation between plasma hormone profiles, symptoms, and response to oestrogen treatment in women approaching the menopause. 21 37

It has been demonstrated that 5.0 mug estradiol-17beta (E2) iv inhibits spontaneous episodic release (SER) of LH from 3-9 h after injection in immature female pigs (gilts). To understand this phenomenon we tested pituitary response (PR) to synthetic LH-RH/FSH-RH (LH-RH) for 13 h after identical E2 treatment in eight 7-8-week-old gilts. Using chronic cannulae PR was determined by measuring the change in plasma LH (delta LH) by RIA after iv injection of 2.0 mug LH-RH. PR was determined every 2 h starting 1 or 2 h before E2 or saline treatments. The PR prior to treatment was 4.3 plus or minus 0.3 ng/ml. By the second releasing-hormone challenge PR in controls was depressed, remaining at about 2.5 ng/ml thereafter. Compared with controls PR depression was greater (P less than 0.005) 1 h following E2 (delta LH = 1.0 plus or minus 0.4 ng/ml). Responsiveness then returned toward pretreatment levels and from 6 h post-treatment onward PR was not different from controls. Initial inhibition of SER may therefore be located in the pituitary and brain. However, after 4 h inhibition appears to be purely neural. Earlier studies showed that subcutaneous (SC) implants of E2 for 3 days in prepubertal gilts depressed PR to LH-RH. We further examined the effect upon PR of implants releasing physiologic levels of E2. PR was evaluated as above at 2-h intervals for 12 h after SC implantation of silastic capsules containing E2 (n = 6) or sham implant (n = 1); then every 6 h up to 54 h post-treatment. For the first 12 h PR depression in the control was identical to controls in the acute experiment; after 36 h PR was similar to pretreatment levels. In E2 implanted animals PR fell to a mean of 1.8 plus or minus 0.1 ng/ml, 4-12 h after implantation, then recovered, stabilizing at 2.3 plus or minus 0.1 ng/ml after 18 h. It is concluded that estrogen treatment rapidly causes a depression of pituitary response to exogenous LH-RH. This rapid effect may not be dependent on E2 dosage. The extent of recovery of pituitary responsiveness probably depends upon the level and persistence of the E2 treatment.
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PMID:Acute and chronic estradiol-17beta inhibition of LH release in prepubertal female pigs: time course and site of action. 23 35

Multiple sampling was carried out in 4 postmenopausal women for measurement of LH and FSH before and at the end of a 1-week treatment period with Danazol (400 mg daily). A small but significant depression of FSH was found in 3 of 4 subjects, while a significant depression of LH was only seen in 1 subject. In view of the very modest gonadotrophin suppression demonstrated in these women it is possible that Danazol also exerts its profound and sometimes rapid effects through inhibition of positive oestrogen feedback and by direct actions on the ovaries and endometrium.
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PMID:Effects of Danazol on pituitary gonadotrophins in post-menopausal women. 28 68

This study was designed to assess the effect of long-term treatment with three combined oral contraceptives (OC) on the gonadotropin response to LHRH. The release of LH and FSH after a single 50-microgram dose of LHRH was studied from Days 11 to 14 of treatment and Days 2 and 3 after discontinuation of the treatment. The responses were compared with controls during the luteal phase (Days 16 to 19) of the menstrual cycle. LH and FSH baseline levels and release after LHRH injection were markedly depressed in women on OC treatment. The patterns of gonadotropin response after LHRH, however, were similar to the responses during the luteal phase. Following discontinuation of OC treatment, the basal levels of LH and FSH and the response to LHRH continued to be depressed, with a further decrease in the FSH release. These results indicate that treatment with combined OC exert a significant depression on the release of gonadotropins.
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PMID:The effect of oral contraceptives on the gonadotropin response to LHRH. 36 56


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