Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.25.1 (proteasome)
28,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven female patients with amenorrhea, galactorrhea, and hyperprolactinemia were examined before and after selective transsphenoidal removal of a PRL-secreting microadenoma. Before adenomectomy, metoclopramide (MCP; 10 mg orally) and TRH (200 micrograms iv) did not increase PRL blood levels in any of the seven patients. On the contrary, after oral administration of 10 mg MCP, a positive response was noted in a group of eight lactating women 3 days postpartum. After surgery, serum PRL level returned to normal in all patients. A positive PRL response to MCP and TRH was found in six of the seven patients 1 month after surgery. One patient, who had the lowest PRL level, failed to show a PRL increase after both stimuli. These findings indicate that hypothalamic pituitary function can be restored to normal after transsphenoidal removal of PRL-secreting pituitary tumors.
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PMID:Serum prolactin response to thyrotropin-releasing hormone and metoclopramide in patients with prolactin-secreting tumors before and after transsphenoidal surgery. 12 21

Dopaminergic and serotoninergic systems are involved in regulation of prolactin (PRL) and TSH secretion. About 10% of patients presented because of an galactorrhea and hyperprolactinemia (HP) have uncompensated primary hypothyroidism (PH). Two groups of patients were investigated using metoclopramide (MCP, DA antagonist, 10 mg i.v.), cyproheptadine (serotonin antagonist, 4 mg per os) and TRH tests. Group A consisted of 12 females with PH and hyperprolactinemia (HP). Group B presented 4 females with PH, HP and pituitary microadenoma on CT-scan. In control group of healthy euthyroid women basal PRL and TSH levels were in the normal range and statistically significant increase of both hormones was observed after MCP and TRH injections. Marked increase of basal TSH and PRL levels was found in both clinical groups. In contrast to control group no TSH reaction in MCP test was observed. PRL response to MCP was declined in group B versus group A. Cyproheptadine inhibited TSH secretion in patients with HP and PH, while this effect was absent in control group. TRH stimulated TSH and PRL response in group B was declined. Presented data shows that HP in PH may be due to the presence of subclinical microadenoma made manifest by hypothyroid state and/or due to disturbances in monamine control of PRL and TSH secretion.
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PMID:Monoamine regulation of prolactin and TSH secretion in hypothyroidism. 151 63

Of 210 women with galactorrhea 66.2% had normal prolactin serum levels. Only in 33.4% elevated prolactin levels could be found, 0.4% were hypoprolactinemic. The TRH-stimulation test detected latent hyperprolactinemia in 13.5% of the cases, showed a normal thyroid function in 81.5%, hypothyroidism in 13.9% and hyperthyroidism in 4.6% and this is considered to be a more valuable diagnostic tool than the MCP-test. Galactorrhea was associated with the following conditions: hyperprolactinemia (34.8%), menstrual disturbances (67.4%), post-pill amenorrhea (30.2%), mastalgia (30.2%), prolactinoma (18.6%), fibrocystic disease (11.6%), hirsutism (4.6%), diabetes mellitus (2.3%).
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PMID:[The value of hyperprolactinemia determination within the scope of galactorrhea]. 249 8

Pre- and postoperative hypothalamic-pituitary-thyroid axis function was studied in 38 patients with pituitary adenomas (PRL, GH and ACTH tumours), of whom 35 were surgically confirmed and three diagnosed by clinical signs, CT scanning and hormone assessments. About ten days after operation, the same study was repeated in 10 patients with prolactinoma and 7 with growth hormone (GH) tumour. The preoperative abnormal serum TSH response to TRH was found in 8/20 patients with prolactinoma, 9/16 with GH tumour, and 2/2 with Cushing's disease due to ACTH microadenoma. The incidence of abnormal TSH response to TRH was not significantly increased in patients with larger adenoma in either PRL or GH tumour group. In 8 cases of prolactinoma, metoclopramide (MCP, 10 mg, P.O.) test was also performed and there was a significant positive correlation between TSH responses to TRH and to MCP. Serum TT3 in the GH tumour group was within normal ranges, but significantly higher than that of the normal and prolactinoma groups. After operation, TT3 was significantly decreased as compared with that before operation and there were marked changes in TSH response to TRH. In conclusion, there were some abnormalities in TSH control in patients with non-TSH pituitary tumour, and in serum TT3 control in patients with GH tumour. The surgical treatment of pituitary adenoma can lead to transient decrease in TSH reserve and serum TT3 level probably resulting from both stress and/or destruction of thyro-trophs by the operation.
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PMID:Pre- and post-operative hypothalamic-pituitary-thyroidal axis function in patients with prolactinoma, growth hormone tumour and ACTH tumour. 255 2

In order to establish the influence of dopaminergic, alpha-adrenergic and cholinergic pathways on GRF-mediated GH release we have studied the GH responses to GRF 1-29 (100 or 50 micrograms as i.v. bolus) alone and in combination with metoclopramide (MCP, 10 mg, i.v.), thymoxamine (THYM, 210 micrograms/min, 150 min infusion), and atropine (1.2 mg, i.v.). We have also investigated any possible interaction between TRH and GRF in view of the reported inhibitory effects of TRH infusion on stimulated GH release. Dopaminergic and alpha-adrenergic blockade with MCP and THYM respectively, did not have any effect on the GH responses to GRF. This lack of effect strongly suggests that any action which these neurotransmitters may exert on GH secretion is not at a pituitary level. TRH did not modify the GH response to GRF suggesting that the inhibitory effect on stimulated GH secretion is exerted at a hypothalamic level. In contrast, GH responses to GRF were significantly reduced by prior administration of atropine. These data support the view that cholinergic pathways play an important role in the regulation of GH secretion and such control may be exerted at both hypothalamic and pituitary levels.
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PMID:Influence of dopaminergic, adrenergic and cholinergic blockade and TRH administration on GH responses to GRF 1-29. 287 52

Studies were undertaken to evaluate the effects of cysteamine (CSH), cystamine (CS-S), N-acetyl-cysteine, D-penicillamine, and a major metabolite of CSh, taurine, on plasma PRL levels in normal and estrogen-primed hyperprolactinemic rats. Both CSH and CS-S caused a marked decrease in plasma PRL concentration in hyperprolactinemic rats. The effects of CSH and CS-S lasted for at least 6 h but returned toward pretreatment levels 24 h later. In normal rats a fall in basal plasma PRL concentration was not readily observed but after stimulation with TRH or metaclopramide, PRL secretion elicited by these stimuli was markedly inhibited by CSH and CS-S. The response to TRH or MCP 24 h after treatment with CSH was variable with CS-S appearing to cause an unexpected increase in PRL release in response to TRH or metaclopramide. The structurally related compounds, taurine, N-acetyl-cysteine, and D-penicillamine did not cause any reduction of plasma PRL levels in hyperprolactinemic rats. This may be due, in the case of taurine, to a loss of the free sulfydryl group, in the case of N-acetyl-cysteine, a change in basicity because of a carboxyl group and derivatization of the amino group and D-penicillamine, again a change in basicity due to a free carboxyl group as well as an altered structural relationship between the free amino and sulfydryl groups. These studies indicate that CSH and CS-S by possible reduction to CSH cause a reversible depletion in plasma PRL in normal and hyperprolactinemic rats. Because both substances inhibit different receptor-mediated stimuli, their mechanism of action is likely to be mediated at a common locus involved with the synthesis and release of PRL.
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PMID:The effect of cysteamine, cystamine, and the structurally related compounds taurine, N-acetyl-cysteine, and D-penicillamine on plasma prolactin levels in normal and estrogen-primed hyperprolactinemic rats. 310 88

Prolactin dynamic was investigated in 43 premenopausal patients with primary empty sella (PES) diagnosed by pneumoencephalography and CT scan. Only normoprolactinemic patients were included in this study. Basal PRL levels ranged from 4 to 25 ng/ml. PRL responses to TRH (200 micrograms i.v.) and metoclopramide (MCP, 10 mg p.o.) were not significantly different from those in normal subjects, although a trend toward higher responses was present in PES patients. The administration of nomifensine (NOM, 200 mg p.o.) induced a PRL decrease, which was not significantly different from that in normal subjects. However, a sequential stimulation with TRH plus MCP (1 h after TRH administration) induced an exaggerated PRL increase which was significantly different from that in normal subjects. The peak PRL responses after stimulation were not significantly correlated with estradiol levels or FSH/LH ratios in our patients. The influence of body weight was also excluded on the basis of the responses observed in 8 obese control subjects that were significantly lower than in PES patients. Moreover, in 19 patients we studied the intracranial pressure (ICP) through an indwelling catheter inserted into the lumbar subarachnoid space. ICP was normal in 5 patients and elevated in 14 patients. When we compared PRL dynamics in patients with normal or elevated ICP, a significant difference was noted between the percentage of PRL decrease after NOM, that was lower and delayed in patients with increased ICP, suggesting an influence of ICP on neuronal dopamine reuptake. In conclusion, an augmented PRL reserve is present in premenopausal patients with PES. A correlation can be found between ICP and the function of dopaminergic neurons controlling lactotroph cells.
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PMID:Prolactin dynamics in normoprolactinemic primary empty sella: correlation with intracranial pressure. 312 88

It has previously been demonstrated in our laboratory that patients with pseudohypoparathyroidism (PsHP) have impaired PRL responses to TRH and chlorpromazine. We have also observed that these patients have low basal plasma renin activity (PRA) and decreased aldosterone responses to upright posture and isometric handgrip exercise. Since inhibitory dopaminergic modulation of PRL and aldosterone is well established, we have examined whether PsHP is associated with altered dopaminergic inhibition of PRL and aldosterone secretion. To investigate this possibility, we compared the plasma PRL, aldosterone, and PRA responses to the dopamine antagonist metoclopramide (MCP; 10 mg iv) in seven normocalcemic PsHP patients and twelve normal controls. These patients were on no medications except calcium and vitamin D for 2 weeks; they were maintained on a diet containing 50 meq of sodium and 80 meq of potassium for 5 days. Although basal PRL levels were similar in the two groups of subjects, the maximal incremental PRL response in PsHP patients (38.7 +/- 12.6 ng/ml) was less (P less than 0.01) than in normal subjects (61.6 +/- 9.6 ng/ml). Basal supine plasma aldosterone was less (P less than 0.01) in PsHP patients (8.0 +/- 1.1 ng/dl) than in normal subjects (13.4 +/- 2.1 ng/dl). Maximum incremental aldosterone response to MCP (8.7 +/- 1.9 ng/dl) in PsHP patients was also less (P less than 0.01) than in normal subjects (13.4 +/- 2.1 ng/dl). Basal supine PRA was lower (P less than 0.05) in PsHP patients (1.3 +/- 0.3 ng/ml.h) than in normal subjects (2.8 +/- 0.4 ng/ml.h). However, the PRA responses to MCP were similar in both groups. Tonic dopaminergic inhibition of PRL and aldosterone secretion, but not renin secretion, appears to be less pronounced in PsHP patients. This is the first disease state in which reduced aldosterone responses to dopamine antoganism have been observed. Decreased PRL and aldosterone responses to MCP may reflect decreased ambient dopamine levels and/or a reduction in dopamine receptor number or binding affinity.
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PMID:Altered dopaminergic modulation of prolactin and aldosterone secretion in pseudohypoparathyroidism. 701 87

To evaluate the acute effect of human erythropoietin (r-HuEPO) on basal and stimulated prolactin (PRL) secretion, 18 normal subjects (12 females, 6 males) were studied. The PRL response to thyrotropin-releasing hormone (TRH; 200 micrograms intravenously, n = 7), metoclopramide (MCP, 20 mg intravenously, n = 5) and fenfluramine (FF, 60 mg os, n = 6) was tested in presence of saline or r-HuEPO (30 U/kg intravenously). The drug neither modified basal PRL levels nor affected the normal PRL release to TRH, MCP and FF. Our results indicate that, in normal subjects, the acute administration of therapeutic doses of r-HuEPO does not interfere with PRL secretion both after a direct pituitary stimulus and after stimuli involving dopaminergic and serotoninergic pathways.
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PMID:Effects of erythropoietin administration on prolactin secretion in normal subjects. 830 3

It is widely accepted that, in man, galanin, a neuropeptide, has a clear GH-releasing effect while its stimulatory influence on PRL secretion is matter of debate. To clarify this point, in 6 normal young women (23-35 yr) in their early follicular phase, we studied the effect of galanin (pGAL, 80 pmol/kg. min infused i.v. over 60 min) on both basal and arginine (ARG, 0.5 g/kg i.v. in 30 min), TRH (400 micrograms i.v. as a bolus at 0 min) or metoclopramide (MCP, 10 mg i.v. as a bolus at 0 min)-stimulated PRL secretion. GAL infusion failed to significantly increase basal PRL levels (peak vs baseline: 12.2 +/- 3.6 vs 8.7 +/- 1.2 micrograms/L) but counteracted the spontaneous PRL decrease observed during saline infusion (AUC: 1216.6 +/- 282.1 vs 672.0 +/- 94.5 micrograms.min/L; p < 0.05). GAL infusion clearly enhanced the PRL response to TRH (AUC: 5806.3 +/- 743.0 vs 3952.1 +/- 423.9 micrograms.min/L, p < 0.05) and ARG (AUC: 3676.8 +/- 382.6 vs 2638.9 +/- 287.0 micrograms.min/L, p < 0.05), respectively. On the other hand, GAL failed to modify the MCP-induced PRL response (AUC: 15409.5 +/- 2085.3 vs 14,787.9 +/- 2045.5 micrograms.min/L). The PRL response to MCP was higher than that to TRH (p < 0.01) which, in turn, was higher than that to ARG (p < 0.01). During GAL infusion, the PRL response to TRH or ARG remained lower (p < 0.01) than that after MCP administration. Thus, in conclusion, present data demonstrate that in normal women galanin enhances the PRL response to ARG and TRH but fails to modify that induced by dopamine receptor blockade with metoclopramide. Based on evidence that the inhibition of central dopaminergic activity inhibits the lactotrope responsiveness to dopaminergic antagonists or TRH, it is unlikely that galanin influences PRL secretion via inhibition of dopaminergic tone.
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PMID:Galanin positively modulates prolactin secretion in normal women. 906 7


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