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)

Corticotropin releasing factor (CRF) is a newly sequenced peptide first isolated from sheep hypothalami and thought to be an important modulator of both the pituitary-adrenal axis and the sympathetic nervous system. We administered intravenous, intramuscular, and intracerebroventricular CRH to non-human primates and measured plasma ACTH, beta endorphin, cortisol, GH and PRL responses to CRF. In addition, we determined the pharmacokinetic properties of I125 in these primates. We administered CRF as an intravenous bolus or as a continuous infusion to normal volunteers and as an intravenous bolus to patients with disorders of the hypothalamic-pituitary-adrenal axis, such as Cushing's syndrome and adrenal insufficiency, and patients with endogenous depression and mild hypercortisolism, and assessed their plasma ACTH, cortisol, GH and PRL responses. In addition, we determined the pharmacokinetic properties of CRF in man by measuring CRF immunoreactivity in plasma. CRF given intravenously to primates or man is a slowly metabolized, long-acting, secretagogue of ACTH, beta-endorphin and cortisol. When given intracerebroventricularly to primates it stimulates the hypothalamic-pituitary-adrenal axis without escaping into the plasma and it is actively cleared in the CNS. It does not cross the blood brain barrier appreciably when given intravenously. CRF given to primates and men as an intravenous continuous infusion has only mild ACTH stimulating effects and this may be due to an intact cortisol negative feedback system. Finally, CRF causes characteristic plasma hormone responses in patients with Cushing's disease, adrenal insufficiency and depression.
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PMID:Corticotropin releasing factor: basic studies and clinical applications. 299 71

M-Chlorophenylpiperazine (m-CPP) produces effects on the central serotonergic system in animals compatible with direct agonist activity on postsynaptic serotonin receptors. Although it is a metabolite of the antidepressant trazodone, m-CPP has not previously been given to humans. To evaluate the neuroendocrine, behavioral, and physiological effects of m-CPP, 15 normal subjects were given 0.5 mg/kg m-CPP, orally. Administered acutely under double blind, placebo-controlled conditions, m-CPP was well tolerated by 14 of the 15 subjects; it produced significant increases in plasma PRL and cortisol and in body temperature, without changing pulse or blood pressure. The mean (SD) maximal increases over baseline for PRL, cortisol and temperature were 13.4 (9.9) ng/ml, 10.1 (6.7) micrograms/100 ml, and 0.4 (0.2) C, respectively. A small but significant increase in self-rated activation-euphoria and anxiety was noted by some subjects, whereas there were no significant effects on ratings of depression, dysphoria, altered self-reality, or functional impairment. These results are similar to those for other serotonin agonists and, thus, suggest that m-CPP merits further study as a pharmacological probe of serotonergic responsivity in humans. The results also support the hypothesis that serotonin plays a role in the regulation of PRL, cortisol, body temperature, and mood.
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PMID:Neuroendocrine effects of M-chlorophenylpiperazine, a serotonin agonist, in humans. 405 85

Female dysendocrine sterility has displayed a statistical incidence of 3.4% since 1967 in Milan's fertility and sterility centres. It is always marked by clear-cut clinical situations. Of these, particular interest is attached to anovulation (62.4% of cases), both with the cycle and with anovularity, ovarian micropolycystosis (2.7%), both as Stein ovary and as micropolycystic ovary, disturbances of ovary endocrine secretion: lutein deficiencies (21.2%) in the form of both brief and inadequate luteal phase. Treatment is aimed at possibly discontinuous reinstatement of ovulation. Clinical and pharmacological experiments over the last twenty years have put forward many "inducers". Mention is made of four personal approaches: --clinical employment of homologous gonadotropins (hMG + hCG), sequentially rather than paired, when poor gonadotropin secretion accompanied by insufficient endogenous oestrogenic activity is the main feature. Investigation from June 1964 to December 1981, coupled with monitorisation and personalisation of the treatment, initially through daily checks of total and fractionated oestrogenuria, and in recent years preferably through plasma 17-beta oestradiol or urinary enzyme determinations, has given a different slant to the reported disadvantages of gonadotropic management: hyperstimulation frequent multiple pregnancies, frequent multiple miscarriages; --employment of GnRH or its analogues (indications virtually those for paired gonadotropins). Some uncertainties however, exist with regard to the contraceptive action displayed by the agonist and antagonist analogues at certain doses, and with regard to the antigonadic action GnRH appears to have, both in the depression of oestrogen and progesterone production and in the arrest of follicular maturation an ovulation; --a preference for clomiphene among the antioestrogens in cases of primarily hypothalamic dysfunction and in ovarian micropolycystosis, provided endogenous oestrogenic activity is within normal limits; --a preference for hypoprolactinaemic drugs (bromoergocriptine, lysuride) in PRL-dependency, marked solely by an appreciable increase in serum LTH, screened as functional by means of selective tests; --experimentation of epimestrol, mainly in cases of sterility due to lutein deficiency.
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PMID:[Indications for hormone therapy of female secretory sterility]. 634 86

Gonadotropin responses to GnRH and PRL responses to TRH and metoclopramide (MTC) were investigated in nine consecutive women with amenorrhea and insulin-treated diabetes mellitus. Nine normal menstruating diabetic women, 12 normal women in the early follicular phase, and nine consecutive nondiabetic women with functional amenorrhea served as controls. No significant differences were found in relation to diabetes regulation within the two diabetic groups. Amenorrheic patients with diabetes mellitus had significantly lower basal PRL levels than normal women and estradiol levels compared to the other groups. Basal plasma LH concentrations were significantly lower in women with amenorrhea and diabetes mellitus than in nondiabetics with amenorrhea, whereas plasma FSH levels were similar in all groups. The LH response to GnRH was significantly lower in amenorrheic patients with diabetes mellitus than in normal women, and a significant correlation (r = 0.81, P less than 0.01) was found between the LH response to GnRH and the basal estradiol level in these women. The FSH response to GnRH and the PRL response to TRH were similar in all groups. Amenorrheic diabetics had significantly lower PRL responses to MTC compared to other groups, and nondiabetics with amenorrhea had significantly lower PRL response than normal women. It is concluded that diabetic patients with functional amenorrhea have low basal and MTC-stimulated PRL levels, low basal LH levels, and decreased LH response to GnRH despite low estrogen levels. These hormonal changes may in part be caused by a raised central dopaminergic activity leading to a depression of pituitary ovulatory mechanisms.
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PMID:Gonadotropin responses to gonadotropin-releasing hormone and prolactin responses to thyrotropin-releasing hormone and metoclopramide in women with amenorrhea and insulin-treated diabetes mellitus. 640 66

Superfusion of rat anterior pituitary cell aggregates with 10-min pulses of 0.1-10 nM angiotensin II (AII) resulted in a prompt and concentration-dependent rise of PRL release. The effect could be blocked by saralasin, an AII receptor antagonist. The response to AII, but not that to TRH, was rapidly desensitized: a 10 nM AII pulse caused an 80% depression of the response to a subsequent 10 nM pulse given 50 min later. The data provide a possible functional significance for the renin-angiotensin system recently demonstrated in the anterior pituitary.
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PMID:Stimulation of prolactin release by angiotensin II in superfused rat anterior pituitary cell aggregates. 641 Feb 99

The 24-h mean plasma concentrations of 8 hormones were measured in 11 men with chronic uremia and 32 normal men. Our findings confirm previous reports of subnormal levels of testosterone, T3, and T4 and elevated levels of LH, PRL, and cortisol. In addition, we observed a new finding: markedly subnormal levels of the adrenal androgens dehydroisoandrosterone (DHA) and DHA sulfate. The mean DHA level in the patients was 164 +/- 46 (SD) ng/dl, compared with 320 +/- 124 in age-matched controls (P < 0.0001); the geometric mean DHA sulfate level was 40 micrograms/dl (95% confidence limits, 11-113) in the patients and 76 micrograms/dl (95% confidence limits, 26-214) in age-matched controls (P = 0.005). The depression of adrenal androgen levels in the face of elevated cortisol levels suggests a biosynthetic block in the adrenal cortex at the step where the C-19 and C-21 pathways diverge, namely the removal of the 2-carbon side chain by C-17, 20-lyase. If a similar defect were present in the testes, it could account for the diminished synthesis of testosterone, which is a further metabolite of DHA in the testes.
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PMID:Subnormal plasma adrenal androgen levels in men with uremia. 644 61

This study was designed to more selectively investigate the dopaminergic regulation of 18-hydroxycorticosterone (18-OHB) and aldosterone production by the adrenal zona glomerulosa. Mature rhesus monkeys received either an infusion of dopamine (2 micrograms/kg/min) or 5% dextrose (0.2 ml/min) over a 60 min period (N=6). Dopamine had no effect on plasma levels of renin activity, cortisol, corticosterone, aldosterone or blood pressure. However, dopamine suppressed (p less than 0.05) plasma 18-OHB levels from a baseline of 31.6 +/- 3.5 ng/dl to 23.6 +/- 2.1 ng/dl at 60 min after onset of infusion. This observation is in agreement with some studies in humans but differs from others in which no depression in 18-OHB was observed following dopamine infusion. Dopamine infusion markedly (p less than 0.001) suppressed plasma PRL levels by 30 min after onset of infusion. Corticosteroid responses to metoclopramide (200 micrograms/kg) after dexamethasone 1 mg im every 6 h X 5 days or placebo treatment (vehicle im every 6 h X 5 days) was then evaluated. Dexamethasone significantly suppressed basal cortisol, corticosterone, 18-OHB and aldosterone. Although dexamethasone blunted the prolactin response, it did not inhibit the aldosterone response to metoclopramide. The 18-OHB response to metoclopramide was increased (p less than 0.01) following dexamethasone treatment. Following dexamethasone suppression, 18-OHB levels were still lowered (p less than 0.05) by dopamine infusion. These results suggest that dopamine selectively inhibits zona glomerulosa production of 18-OHB and aldosterone in rhesus monkeys.
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PMID:Evidence for direct inhibitory effects of dopamine on zona glomerulosa secretion of 18-hydroxycorticosterone in rhesus monkeys. 672 68

Male and female hamsters were maintained on a long photoperiod (14L:10D) and were divided into the following groups: group 1, injected with vehicle at both 11.00 and 17.00 h; groups 2-5, injected with various doses of melatonin at 11.00 h (0, 100 micrograms, 500 micrograms, 1 mg) and 25 g of melatonin at 17.00 h. In males, a.m. vehicle p.m. melatonin treatments for 70 days led to atrophy of the testes and accessory sex organs and to a significant depression of both plasma LH and PRL titers. There was a graded inhibition of these actions of exogenous melatonin in animals receiving 100 micrograms, 500 micrograms or 1 mg a.m. injections of melatonin with 1 mg completely preventing the effects of p.m. melatonin. 80% of the female hamsters receiving daily p.m. injections of melatonin for 9 weeks became acyclic with significant decreases in uterine weight and increases in ovarian weight. All doses of melatonin given at 11.00 h suppressed the inhibitory actions of p.m. melatonin with the exception of vaginal cyclicity for which 500 micrograms or more was required to restore normal vaginal cyclicity in all animals. These results demonstrate that morning injections of melatonin can prevent the antigonadotropic effects of afternoon melatonin injections and provide support for the hypothesis that the paradoxical actions of melatonin may be related to the ability of the indole to regulate its own receptors.
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PMID:Influence of morning melatonin injections on the antigonadotrophic effects of afternoon melatonin administration in male and female hamsters. 679 Oct 44

Endocrinological investigation of depressed patients shows a wide variety of abnormalities, most of them reflecting disturbed hypothalamo-hypophyseal control mechanisms. Reported results however vary widely among investigators reflecting the heterogeneity of the clinical cases and the difficulties of quantifying depression. The authors report data on 1(0) TSH, PRL and HGH secretion after TRH in a group of 19 endogenous depressed patients; 2(0) insulin secretions after a glucose load in endogenous (10 cases) and neurotic (13 cases) depression; 3(0) LH and FSH secretion after LHRH in 10 neurotic depressed men. The results are compared with those reported in the literature. Their possible contribution to the differential diagnosis of neurotic versus endogenous depression is discussed.
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PMID:[Endocrinological abnormalities in the neurotic states and in depression (author's transl)]. 679 64

A 68-year-old man was hospitalized in August, 1990 with general malaise, loss of energy, poor appetite and severe depression. He had experienced depressed moods, markedly diminished interest, feelings of worthlessness, diminished ability to think, general malaise and muscle weakness beginning in November, 1989. He was treated for depression at another hospital until his emergent admission to our hospital because of difficulty in walking. Laboratory studies disclosed hyponatremia, low plasma ACTH level (4.2 pmol/L), and a low cortisol level (27.6 nmol/L). Rapid ACTH test elicited an increase in serum cortisol from 75.6 nmol/L to 361.2 nmol/L at 30 min. Ovine corticotropin releasing hormone (CRH) did not stimulate secretion of either ACTH or cortisol. Human growth hormone releasing hormone (GRH) together with thyrotropin releasing hormone (TRH) elicited a normal response of TSH and low responses of GH and PRL. The patient's serum autoantibodies to anterior pituitary cell membranes using GH3 rat pituitary cells and AtT-20 mouse pituitary cells were positive. On the basis of these data, the diagnosis of selective ACTH, GH and PRL deficiency was made and thought to have been caused by lymphocytic adenohypophysitis. Following cortisol replacement therapy, he quickly regained his appetite and was restored to a normal mental state of being.
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PMID:Severe depression associated with ACTH, PRL, and GH deficiency: a case report. 795 79


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