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:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of renin, angiotensin I-converting enzyme and angiotensin II detected by immunocytochemistry in the adult male rat anterior pituitary has suggested the existence of a pituitary renin-angiotensin system. To establish another mammalian experimental model we have investigated the presence of renin, angiotensinogen, angiotensin I-converting enzyme, and angiotensin II II in five normal lamb anterior pituitaries by immunocytochemistry after cryoultramicrotomy. Renin, angiotensinogen and angiotensin II immunoreactivities were observed only in cytoplasmic granules of lactotrophs, and the three proteins were found co-localized with prolactin in the same granules by double immunolabelling. No immunoreactive angiotensin I-converting enzyme was observed. These results suggest an activation of renin in the cytoplasmic granules of lactotrophs leading to a local synthesis of angiotensin II. Thus, the lamb anterior pituitary may provide a good experimental model for investigating the possible autocrine action of a local renin-angiotensin system on prolactin release in the human pituitary.
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PMID:Presence of renin, angiotensinogen, angiotensin II in the lamb anterior pituitary gland: immunocytochemical study after cryoultramicrotomy. 185 10

Recent studies have shown a possible role of different factors in the regulation of prolactin secretion. In fact many neurotransmitters (dopamine) and peptides can modulate prolactin release from anterior pituitary lactotrophs. In vitro and in vivo studies, Angiotensin II has been shown to increase prolactin release. On the basis of these data we have studied the effects of enalapril (ACE-Inhibitor) on baseline plasma prolactin in nine hypertensive post-menopausal women. The results indicate that 15-day inhibition of angiotensin-converting enzyme by enalapril significantly reduced serum prolactin levels. These data suggest that the Angiotensin II may play a role in the control of prolactin secretion in hypertensive women.
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PMID:[Regulation mechanisms in prolactin secretion. Possible role of the hypophyseal renin-angiotensin system]. 223 77

Angiotensin II stimulates prolactin release both in vivo in the rat and in vitro in anterior pituitary cell cultures. Moreover, angiotensin II binding sites have been identified in pituitary lactotrophs and it has been shown that angiotensin converting enzyme (ACE) is present in rat anterior pituitary. We studied the effect of enalapril, a potent converting enzyme inhibitor, on baseline prolactin levels in nine hypertensive postmenopausal women. The results indicate that 15-day inhibition of ACE by enalapril reduced prolactinaemia, suggesting that angiotensin II plays a role in the control of prolactin secretion in hypertensives.
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PMID:Enalapril decreases plasma prolactin levels in hypertensive patients. 256 Mar 16

Enalapril is a long-acting, sulphydryl-free, ACE inhibitor whose humoral and hypotensive effects are maximal at 4-8 h and remain detectable at 24 h after a single dose. Serum profiles after chronic dosing of enalapril show little accumulation of the active diacid metabolite, enalaprilat. Comparison between the observed and predicted steady-state urinary recoveries of enalaprilat yields an effective accumulation half-life of approximately 11 h. In normotensive subjects, enalapril increases renal blood flow whilst leaving glomerular filtration unchanged irrespective of the state of sodium balance. Similarly under conditions of salt loading and salt depletion, a biphasic saluretic response is seen which parallels the excretory maxima for unchanged enalapril (1-2 h) and enalaprilat (4-8 h) suggesting direct interference by the drug moieties with tubular NaCl reabsorption. During the period of maximal enalapril action, uricosuria and phosphaturia are seen, supporting a direct action of enalaprilat on proximal tubular handling of these anions. Detailed documentation of the chronic metabolic effects of enalapril remains incomplete. A small rise in plasma potassium concentrations can occur but overt hyperkalaemia is unlikely in the absence of gross renal failure. Continued dosing is associated with a fall in plasma uric acid concentrations; plasma prolactin concentrations remain unaltered.
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PMID:Kinetic and metabolic aspects of enalapril action. 610 Aug 75

In superfused anterior pituitary reaggregate cell cultures angiotensin II (AII) stimulated both spontaneous and dopamine-inhibited prolactin (PRL) release from subnanomolar concentrations. Angiotensin I (AI) and angiotensin III (AIII) also stimulated PRL release. The magnitude and rate of response to AI was equal to or only slightly lower than that to AII. However, the angiotensin converting enzyme (ACE) inhibitors captopril and teprotide (1 microM) completely abolished the PRL response to 0.1 nM AI and strongly reduced that to 1 nM AI. The intrinsic activity of AIII was lower than that of AII but could be enhanced by adding 2 microM of the aminopeptidase inhibitor amastatin to the superfusion medium. After withdrawal of AIII, PRL secretion rate rapidly returned to baseline levels, whereas after withdrawal of AI or AII, secretion fell to a level remaining significantly higher than basal release. The present findings indicate that stimulation of PRL release by AI is weak unless it is converted into AII by ACE and that aminopeptidase may be important in determining the magnitude and termination of the PRL response. Furthermore, the active peptides induce a different pattern of response.
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PMID:Stimulation of spontaneous and dopamine-inhibited prolactin release from anterior pituitary reaggregate cell cultures by angiotensin peptides. 637 46

Prolactin is an important regulator of prostate citrate production. In rats this regulatory effect of prolactin is specific for lateral prostate, and has no effect on either ventral or dorsal prostate. The mechanisms by which prolactin regulates prostate citrate production have not been elucidated. Two key regulatory enzymes involved in citrate synthesis by prostate epithelial cells are mitochondrial aspartate aminotransferase (mAAT) which provides oxalacetate, and PDH E1 alpha (pyruvate dehydrogenase) which provides acetyl CoA for citrate synthesis. Our previous studies demonstrated that prolactin regulates mAAT. However, an increase in citrate synthesis would require an increase in both oxalacetate and acetyl CoA. Therefore, we investigated the possibility that prolactin might also regulate PDH E1 alpha in LP epithelial cells. The present studies demonstrate that prolactin administration (1 mg/rat) to rats resulted in an increased level of E1 alpha in LP epithelial cells within 6 hr, but had no effect on the E1 alpha level of VP epithelial cells. In vitro studies demonstrated that exposure of freshly prepared LP epithelial cells to prolactin (0.1-1.0 microgram/ml) resulted in increased levels of E1 alpha. Prolactin had no effect on either VP or DP epithelial cells. The stimulatory effect of prolactin on E1 alpha was inhibited by actinomycin and cycloheximide, thereby indicating that prolactin stimulated the biosynthesis of E1 alpha. The studies reveal that prolactin specifically stimulates E1 alpha levels of LP epithelial cells, whereas testosterone specifically stimulates E1 alpha levels of VP epithelial cells. At this time, we propose that the effects of prolactin and testosterone involve increased expression of the E1 alpha gene of LP and VP epithelial cells, respectively.
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PMID:Prolactin specifically increases pyruvate dehydrogenase E1 alpha in rat lateral prostate epithelial cells. 771 83

Significantly higher values of systolic and diastolic arterial blood pressure as compared to the corresponding control group was found in a group of 31 patients with polycystic ovary syndrome (PCO) of age between 22 and 42 years (mean 34 years). It was demonstrated that the activity of the enzyme converting angiotensin I to angiotensin II (angiotensin converting enzyme, ACE) as determined by the spectrofluorometric method of Friedland and Silverstein did not differ significantly from that found in the control group. No significant correlation was also found between the ACE activity and the concentrations of testosterone, androstenedione, dehydroepiandrosterone, LH, FSH, prolactin and estradiol both in the patients and in the control group.
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PMID:[Activity of the enzyme converting angiotensin I to angiotensin II (ACE) in patients with polycystic ovary syndrome]. 805 88

The effects of chronic sub-lethal doses (7-14 mg kg-1 a day for 15 days) of quinalphos were evaluated in adult male rats for changes in testicular morphology, circulatory concentrations of hormones (LH, FSH, prolactin and testosterone), activities of acetylcholinesterase (AChE) and angiotensin converting enzyme (ACE) as well as metabolism of biogenic amines (dopamine, noradrenaline and 5-hydroxytryptamine (5-HT)) in the hypothalamus and pituitary. Hormones were assayed by radioimmunoassay or chemiluminescent immunoassay (testosterone). The enzymes were estimated after spectrophotometry and the biogenic amines by HPLC-electrochemistry. Sub-lethal chronic administration of quinalphos resulted in: decreased testicular mass and AChE activity in central as well as peripheral organs; increased serum LH, FSH, prolactin and testosterone concentrations; decreased pituitary or increased testicular ACE activity; severe disruption of spermatogenesis with increasing doses of pesticide; and no significant effects on dopamine, noradrenaline or 5-HT concentrations in the hypothalamus or pituitary. Administration of oestradiol (50 micrograms per rat a day) during pesticide treatment resulted in: a significant decrease in the mass of the testis and accessory sex organs; decreases in serum LH, FSH, testosterone concentrations; an increase in prolactin concentration; and a decrease in dopamine or an increase in noradrenaline and 5-HT in the hypothalamus or pituitary. Oestradiol had a marked effect: in pesticide-treated animals, the pesticide effects were significantly reversed. This indicates that in pesticide toxicity, the hypothalamo-pituitary-gonadal axis is operational. Since many of the observed pesticide effects could be inhibited by oestradiol, it is suggested that the pesticide acts directly on the gonadotrophins. In conclusion, quinalphos decreases fertility in adult male rats by affecting the pituitary gonadotrophins.
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PMID:Effects of an organophosphate pesticide, quinalphos, on the hypothalamo-pituitary-gonadal axis in adult male rats. 1079 23

A 54 year old man presented with frontal headaches for one year. A CT scan of the head revealed a pituitary mass. He denied a change in vision or galactorrhea, but did have decreased frequency of erections and a recent episode of renal stones. On physical exam, the cranial nerves were normal. Visual field exam revealed mild bilateral temporal defects. The genitalia were normal and the testes were soft. Laboratory evaluation revealed: Na, 134 mM/l; K, 6.7 mM/l; Cl, 104 mM/l; HCO3, 22 mM/l; BUN, 47 mg/dl; Cr, 8.3 mg/dl; Ca, 12.5 mg/dl; Phos, 5.5 mg/dl; prolactin, 32.0 ng/ml; T4, 4.46 microg/dl; TSH, 2.07 microU/ml; LH, 18.1 mIU/ml; FSH 3.2 mIU/ml; alpha subunit 1.6 ng/ml; testosterone 255 ng/dl; cortisol, 20.3 microg/dl; cortisol after 250 microg cortrosyn, 38.5 microg/dl (time 60 minutes); growth hormone, 1.4 ng/ml; IGF-1, 47 ng/ml; PTH, <1 pg/ml; 25-hydroxyvitamin D, 14 ng/ml; 1,25-dihydroxyvitamin D, 69 pg/ml. These results were felt to be consistent with a non-PTH-mediated hypercalcemia, such as humoral hypercalcemia of malignancy, or a vitamin D-mediated hypercalcemia, such as lymphoma, sarcoidosis or tuberculosis. Head MRI demonstrated a 3.5 x 3.5 x 2.5 cm heterogeneous mass enlarging the sella, deforming the clivus and compressing the cavernous sinus, basilar artery and left side of the optic chiasm. There was a small focus of high signal in the superior part of the mass on the T1-weighted image from either a proteinaceous cyst with early calcium deposition or sub-acute blood. These radiographic findings were felt to be consistent with a pituitary adenoma. The patient was treated with intravenous hydration and thyroxine 50 microg daily and underwent a transsphenoidal resection of the pituitary lesion. Pathologic examination revealed a pituitary adenoma with multiple granulomas and crystalline material; this was consistent with sarcoid within the adenoma. Post-operatively, the serum LH fell to 5.5 mIU/ml. A subsequent transbronchial biopsy revealed multiple non-caseating granulomas. A serum ACE level was elevated at 132.6 U/l. He received oral prednisone 60 mg daily with resolution of the hypercalcemia. Neurosarcoidosis occurs in 5 to 15% of patients with sarcoidosis and can involve the hypothalamus and pituitary gland. This is the first reported case of sarcoidosis occurring within a pituitary adenoma.
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PMID:Sarcoidosis within a pituitary adenoma. 1213 93

Carbendazim (methyl-2-benzimidazole carbamate, MBC) a metabolite of benomyl is one of the most widespread environmental contaminant of major concern to human and animal reproductive health. The present investigation was undertaken to study the impact of carbendazim exposure on Leydig cell functions. Adult albino male rats of the Wistar strain were administered with carbendazim (25 mg/(kg (body weight)/day)) orally for 48 days. The control animals received vehicle (corn oil) alone. Another group of rats were treated with carbendazim and the same was withdrawn for a further period of 48 days. After the treatment period, rats were euthanized and blood was collected for the assay of serum hormones such as luteinizing hormone (LH), prolactin (PRL), testosterone and estradiol. Testes were immediately removed and Leydig cells were isolated in aseptic condition. Purified Leydig cells were used for quantification of steroidogenic enzymes such as 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17beta-hydroxysteroid dehydrogenase (17beta-HSD). Leydig cellular enzymatic antioxidants superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), gamma-glutamyl transpeptidase (gamma-GT), glucose-6-phosphate dehydrogenase (G6PDH) and non-enzymatic antioxidants such as reduced glutathione (GSH), alpha-tocopherol (vitamin E), ascorbic acid (vitamin C) and beta-carotene (vitamin A) were assayed. Lipid peroxidation (LPO) and reactive oxygen species (ROS) were also quantified. Carbendazim exposure had no effect on body weight, serum LH and prolactin. However, testis weight, serum testosterone and estradiol were significantly decreased. In addition to this, Leydig cellular activities of steroidogenic enzymes such as 3beta-HSD, 17beta-HSD, antioxidant enzymes SOD, CAT, GPx, GR, GST, gamma-GT, G-6-PDH and non-enzymatic antioxidants such as GSH, vitamins E, C and A were significantly diminished, whereas LPO and ROS were markedly elevated. All these above-mentioned parameters from the animals after withdrawal of MBC treatment were similar to those of the control group. Thus, the present study suggests that chronic low dose treatment of MBC is capable of inducing reproductive toxicity through increased oxidative stress, but is transient and reversible upon withdrawal of treatment.
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PMID:Modulation of antioxidant defense system by the environmental fungicide carbendazim in Leydig cells of rats. 1748 93


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