Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to identify prolactin-producing tumours in human pituitary glands, 45 chromophobe adenomas, obtained from unselected necropsies, have been studied by various staining procedures including the immunoperoxidase technique for the demonstration of prolactin. The presence of immunoreactive prolactin was revealed in the cytoplasm of the tumour cells in six cases (13%), indicating that the occurrence of prolactin-producing adenomas is not rare. No correlations were established between tumours and clinical history. Two adenomas were detected in female and four in male patients. The age of the patients at necropsy ranged from 28 to 75 years. Three adenomas were associated with disseminated carcinoma, two with fatal liver disease, and one with diabetes mellitus, atherosclerosis, and pyelonephritis. Manifest endocrine symptoms were not disclosed, and endocrine investigations, including measurements of blood prolactin levels, were not undertaken. Thus, direct evidence is lacking as to whether or not these tumours were actively secreting prolactin. In the non-tumorous parts of the anterior lobes the number of prolactin cells was decreased in two cases, suggesting that prolactin released from the adenoma cells suppressed prolactin production in the non-tumorous pituitary. However, the number of prolactin cells of the non-tumorous adenohypophysis seemed to be unchanged in two and increased in another two cases. The present findings conclusively proved the existence of the prolactin-producing adenomas as a distinct entity. These tumours do not stain with acid or basic dyes, they are PAS or thionin negative, and do not contain immunoreactive growth hormone. Thus, by conventional staining procedures they are indistinguishable from other chromophobe adenoma types. Herlant's erythrosin and Brookes' carmoisine methods, claimed spedifically to stain prolactin cells, failed to provide reliable results, hence their use cannot be recommended in tumour identification. Immunoperoxidase staining of prolactin is the only technique which conclusively reveals the presence of immunoreactive prolactin in the cytoplasm of the tumour cells and permits diagnosis. It is proposed that this technique be introduced in pituitary morphological studies. Its application may lead to a better understanding of problems related to prolactin-producing tumours and their secretory activity.
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PMID:Localization of prolactin in chromophobe pituitary adenomas: study of human necropsy material by immunoperoxidase technique. 77 66

Non-arteriosclerotic, virgin and arteriosclerotic breeder rats were subjected to chronic treatment with prolactin or prolactin-releasing drugs such as perphenazine and reserpine for 12 weeks. Males and females responded to the prolactin as evidenced by increased milk secretion, adrenal hyperplasia and thymus gland involution. Although the prolactin- and reserpine-treated animals gained weight and manifested pituitary gland basophilia, the perphenazine-treated animals showed considerable loss of body weight as well as involution of the pituitary gland, ovaries and testes, suggesting a condition of induced hypopituitarism. Chronic treatment with prolactin, both directly and indirectly, caused uniform increases in serum enzymes, e.g., CPK, SGOT, SGPT and LDH, lipids, e.g., triglycerides, free fatty acids and cholesterol, glucose and BUN. Corticosterone production was enhanced by prolactin, reduced by perphenazine and unaffected by reserpine. Prolactin did not induce any arterial disease in the arteriosclerosis-resistant, virgin rats but it did cause eracerbation of the usual severity of arteriosclerosis in the hilar renal arteries of the arteries sclerosis-prone, breeder rats as well as an increased incidence of "old" and "new" foci of myocardial necrosis, characteristically found in breeder rats. It is suggested that hypothalamic control of prolactin as well as ACTH release may play a role in the spontaneous arteriosclerosis which develops in repeatedly-bred, male and female rats.
Atherosclerosis
PMID:Comparative effects of prolactin, perphenazine and reserpine on non-arteriosclerotic (virgin) vs arteriosclerotic (breeder) rats. 94 17

Serum levels of LH and prolactin were measured in repeatedly-bred, arteriosclerotic female rats. Serum LH was abnormally decreased on the afternoon of proestrus and estrus. The extent of the depression of circulating LH levels parallels the severity of the arteriosclerosis. Serum prolactin was significantly increased above normal at proestrus, and the degree of prolactin increase was also correlated with the degree of severity of arteriosclerosis. It is suggested that frequent and repeated pregnancies affect the hypothalamic-pituitary-adrenal-gonadal axis leading to hormonal and metabolic imbalance, which may play a causal role in the pathogenesis of the spontaneous arteriosclerosis which appears in repeatedly-bred rats.
Atherosclerosis
PMID:Changes in LH and prolactin in arteriosclerotic femal breeder rats. 114 28

The authors determined content of steroid hormones (testosterone, estradiol) and gonadotropic pituitary hormones (follicle stimulating, luteinizing, prolactin) in blood plasma by means of radioimmunological assay and evaluated the state of cerebral hemodynamics by results of zonal rheoencephalography in 77 patients with initial manifestation of circulatory brain insufficiency, transient disorders of the cerebral circulation and in the restorative period of stroke against the background of cerebral atherosclerosis. Established was a significant correlation between the content steroid sex hormones and the main quantitative values of the rheoencephalograms of the above patients.
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PMID:[Sex hormones and cerebral hemodynamics in men with cerebrovascular insufficiency]. 141 94

The effects of prolactin (PRL) on A10 (aortic smooth muscle) cell proliferation were examined by measuring both [3H]thymidine incorporation and increases in cell number. PRL induced a significant proliferative response from 10(-11) to 10(-7) M, with optimal activity at 10(-10) M. PRL also enhanced platelet-derived growth factor (PDGF)-induced proliferation. The possibility that PRL induces proliferation through a protein kinase C (PKC)-mediated mechanism was also examined. PRL caused activation of PKC from 10(-12) to 10(-8) M. Antiserum to PRL, a monoclonal antibody directed against the PRL receptor and the immunosuppressive agent cyclosporine A, were able to inhibit PRL-induced proliferation and activation of PKC. The PKC inhibitors, staurosporine, sphingosine, and 1-(-5-iso-quinoline-sulfonyl)-2-methylpiperazine (H-7) also antagonized both proliferation and PKC activation. These data strongly suggest that PRL-induced A10 cell proliferation is mediated through the PKC pathway and that this may play a role in vascular smooth muscle cell hyperplasia, characteristic of the pathogenesis of cardiovascular diseases such as hypertension and atherosclerosis.
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PMID:Prolactin induces proliferation of vascular smooth muscle cells through a protein kinase C-dependent mechanism. 186 Aug 93

Arachidonate 15-lipoxygenase (an n-6 lipoxygenase) has been purified to homogeneity, cloned and expressed and appears to be a highly regulated enzyme showing pronounced tissue specificity. The enzyme is expressed prominently in the reticulocyte where it appears to be under posttranscriptional control and may play a key physiological role in reticulocyte maturation by initiating mitochondrial breakdown. 15-Lipoxygenase is also expressed in significant quantities in airway epithelial cells and eosinophils although no clear role for this enzyme in these cell types has been defined. The enzyme catalyzes the conversion of free arachidonic acid to 15-HPETE, free linoleic acid to 13-HPOD and can also oxygenate polyenoic acids esterified in phospholipids. A number of potential physiological and pathological roles for products of this enzyme have been postulated. These include a physiological role in prolactin secretion from pituitary cells and in the initiation of the acrosome reaction in spermatozoa. An important pathological role in the oxidation of LDL by macrophages has also been proposed, indicating that the enzyme could be a pharmacological target for the treatment of atherosclerosis.
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PMID:Arachidonate 15-lipoxygenase; characteristics and potential biological significance. 191 Aug 64

1. Cysteamine is formed by degradation of coenzyme A (CoA) and causes somatostatin (SS), prolactin and noradrenaline depletion in the brain and peripheral tissues. 2. Cysteamine influences several behavioral processes, like active and passive avoidance behavior, open-field activity, kindled seizures, pain perception and SS-induced barrel rotation. 3. Cysteamine has several established (cystinosis, radioprotection, acetaminophen poisoning) and theoretical (Huntington's disease, prolactin-secreting adenomas) indications in clinical practice. 4. Pantethine is a naturally occurring compound which is metabolized to cysteamine. 5. Pantethine depletes SS, prolactin and noradrenaline with lower efficacy compared to that of cysteamine. 6. Pantethine is well tolerated by patients and has been suggested to treatment of atherosclerosis. The other possible clinical indications (alcoholism, Parkinson's disease, instead of cysteamine) are discussed.
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PMID:Preclinical and clinical studies with cysteamine and pantethine related to the central nervous system. 227 50

In a comparative study the authors determined peripheral blood concentrations of immunoreactive testosterone, estradiol, LH, FSH, and prolactin in 32 males and 21 females, aged 60-74 years, with consequences of ischemic stroke, and in clinically normal elderly subjects. A control group was composed of healthy young people aged 20 to 35 years. It was found that in males and females with a history of stroke secretory insufficiency of the gonads and changes in the gonadotropic function of the pituitary expressed in a relative redistribution of gonadotropin fractions were significantly more pronounced than in normal age-matched subjects. The patients of both sexes exhibited a considerable elevation of blood prolactin levels. Hyperprolactinemia may either follow stroke since the latter impairs the hypothalamic regulation of prolactin secretion or precede it contributing to the development of a metabolic background conducive to the development of cerebral atherosclerosis.
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PMID:[Gonadal and gonadotropic function of late middle-aged men and women with sequelae of ischemic stroke]. 310 53

The role of sex hormones in atherogenesis has not been well defined. Since hemodialysis patients show signs of feminization and an increased propensity for atherosclerosis they are particularly suited to probe the relationship between estrogen, testosterone, and atherosclerosis. Therefore, we measured plasma total, free, and protein-bound estradiol (E2), testosterone (Te), and prolactin in 28 hemodialysis patients and in 30 age-matched controls. Von Willebrand factor (vWF) levels were also assayed. Total and free E2 as well as Te were significantly decreased in the patients (p less than 0.001). However, the E2/Te ratio was elevated in the patients (p = 0.05), as was vWF (p less than 0.01). No correlations were found between hormone levels and vWF, gynecomastia or vascular disease, but vWF and vascular disease were highly correlated. We conclude that in hemodialysis patients absolute estrogen levels are lower than normal, but that the estrogen/androgen ratio is shifted in favor of estrogen because of the coexistence of androgen deficiency. These findings suggest that an elevation in the estrogen/androgen ratio, rather than an increase in estrogen per se, may be a risk factor for atherosclerosis.
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PMID:Plasma estrogens, androgens, and von Willebrand factor in men on chronic hemodialysis. 326 48

The effect of ceruletide (CRL), a synthetic decapeptide analogue of cholecystokinin, on rest pain and arterial blood flow was evaluated in 8 patients with advanced, occlusive atherosclerosis of the lower extremities. CRL 1, 2, or 4 ng kg-1 or placebo were infused intravenously in random order, and in a double-blind fashion. Pain relief, assessed by a scoring system, was significantly better (p less than 0.01) following the 2 and 4 ng kg-1 doses of CRL (2.71 and 2.66, respectively) than following placebo (0.75). Arterial blood flow was not affected by either CRL in any dose or by placebo. Pretreatment with naloxone, a pure opioid antagonist, abolished the analgesic effect of CRL. Following the 2 ng dose of CRL, beta-endorphin levels were significantly elevated from a basal value of 125 +/- 15 pg/ml to 191 +/- 35 pg/ml 5 h after CRL administration (p less than 0.05). Circulating levels of ACTH, prolactin and GH were not affected by CRL. It is concluded that CRL was effective in relieving ischaemic rest pain, and that the mechanism was related to the release of endogenous opioids.
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PMID:Effect of ceruletide on rest pain in patients with arterial insufficiency of the lower extremity. 629 Feb 28


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