Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The evidence that prolactin is a fluid and electrolyte regulator in mammals is reviewed, with particular emphasis on the renal actions of prolactin. Prolactin receptors are found in mammalian kidneys. Prolactin modulates renal formation of cyclic AMP and polyamines and it leads to demonstrable histological changes in the proximal tubules. The renal actions of prolactin primarily involve modulation of the effects of other hormones and are therefore critically dependent on the background physiological situation. Prolactin seems able to cause a prolonged reduction in water, sodium, and potassium excretion, a pattern that is imitated by no other hormone with the possible exception of growth hormone. Prolactin preparations can cause an acute antidiuresis, which may in part be related to contamination of prolactin preparations with vasopressin. However, most of the described effects cannot be explained by vasopressin contamination. This is particularly so with the effects of prolactin on water movements across fetal skin, the amniotic membrane, and in the eye where prolactin and vasopressin have diametrically opposite effects. It is concluded that prolactin is a regulator of fluid and electrolyte metabolism in mammals but that it is a modulator rather than a primary controlling factor.
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PMID:Prolactin as a regulator of fluid and electrolyte metabolism in mammals. 624 16

Deficiencies of corticotrophin (ACTH), growth hormone, and prolactin were documented in a woman with diabetes mellitus and Sheehan's syndrome. The patient's ACTH deficit appeared to be secondary to a hypothalamic abnormality since on two occasions the patient had a marked plasma ACTH response to vasopressin but not to insulin induced hypoglycaemia. It is postulated that the deficits of these three adenohypophysial hormones were instrumental in causing a severely impaired aldosterone secretory capacity in response to sodium restriction and an angiotensin infusion. In addition, the patient had an unusual form of thyroid dysfunction that was in part reversed with hydrocortisone replacement. The patient's unfortunate death during a hypoglycaemic crisis allowed correlation between her extensive antemortum endocrine testing and her pathologic anatomy.
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PMID:Corticotrophin, growth hormone and prolactin deficiencies with hypoaldosteronism and corticosteroid-reversible hypothyroidism in Sheehan's syndrome. Clinical and anatomical correlations. 625 5

Continuous cell lines have been established from a variety of biopsy and postmortem species of tumor from patients with small-cell carcinoma of the lung (SCCL) and have been maintained over several years. The medium from the cultures has been assayed for peptide, glycoprotein, and steroid hormones. Significant amounts of 14 hormones including calcitonin, adrenocorticotropin (ACTH), parathormone, luteinizing hormone, chorionic gonadotropin, glucagon, growth hormone, somatostatin, prolactin, beta-endorpin, lipotropin, oxytocin-neurophysin, vasopressin-neurophysin, and estradiol have been demonstrated. Up to ten different hormones have been produced by a single cell line. Most produce ACTH and all evaluated so far produce estradiol. These studies indicate that cells from SCCL have a potential for producing a wide variety of hormones and that this characteristic can be maintained for prolonged periods of culture in vitro.
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PMID:Hormone production by cultures of small-cell carcinoma of the lung. 626 22

The endocrine status of 106 patients with undifferentiated small cell carcinoma of the lung was evaluated before treatment was begun. Almost one half of the patients had evidence of abnormal control of the secretion of adrenal cortical steroids, manifested by loss of diurnal rhythmicity or dexamethasone suppressibility. Only two had the clinical syndrome of ectopic ACTH secretion. Evidence of inappropriate secretion of vasopressin was found in 38% of the patients, most of whom also had abnormalities of corticosteroid secretory pattern. About one half of the patients had evidence of abnormal glucose tolerance, and many also had a paradoxical rise of plasma growth hormone concentration after glucose administration. The levels of the other hormones studies were normal. The pattern of hormone abnormality observed in these patients appears to be relatively specific for small cell undifferentiated carcinoma, and is different from that observed in other pulmonary tumors. Patients with abnormal control of plasma cortisol had a worse prognosis than those with normal adrenal function, largely because of decreased response rates to chemotherapy. Other endocrine abnormalities were of no prognostic significance.
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PMID:Endocrine function in small cell undifferentiated carcinoma of the lung. 629 25

Opiate receptors in the central nervous system may be classified according to pharmacological, behavioural, or binding studies. Classical mu-receptors probably have beta-endorphin as an endogenous ligand, and seem to be involved in the modulation of pain perception, low-frequency acupuncture analgesia, and the stimulation of prolactin, growth hormone and thyroid-stimulating hormone release. Met-enkephalin is likely to be an endogenous ligand for the delta-receptors, which predominate in the basal ganglia and limbic systems; such receptors may tonically inhibit the release of corticotrophin-releasing factor. It has been suggested that the newly-described kappa-receptors may inhibit the release of vasopressin and gonadotrophin-releasing factor; dynorphin may be their endogenous ligand. Endogenous opiates controlling cardiovascular and respiratory reflexes are likely to activate mu-receptors, while high-frequency acupuncture may alleviate the symptoms of opiate withdrawal by allowing an increase in Met-enkephalin to activate delta-receptors. In the periphery, beta-endorphin is concentrated in the corticotrophs of the anterior pituitary, and is cosecreted with ACTH and related peptides. Circulating Met-enkephalin originates in the gut, sympathetic nervous system and adrenal medulla. Met-enkephalin may also be extracted from carcinoid tumours and phaeochromocytomas. Elevations in circulating Met-enkephalin may occur in certain disease states with cardiovascular and psychiatric manifestations. However, manipulation of endogenous or exogenous opiates has as yet no certain place in any clinical situation.
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PMID:Opiate receptors: enkephalins and endorphins. 630 48

Twelve male volunteers given apomorphine (20 micrograms/kg/hr) for 40 min by i.v. infusion had significant changes in growth hormone, prolactin, vasopressin, pulse rate, sedation and nausea. Naloxone, (20 mg i.v.) or placebo given in a double-blind manner 10 min before the end of the apomorphine infusion as a concealed bolus did not alter the effects of apomorphine. Vasopressin rise correlated significantly with nausea intensity. We conclude that acute opiate receptor blockade does not reverse most apomorphine effects.
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PMID:Failure of naloxone to reverse apomorphine effects in humans. 630 2

The chemical tools that could be used to examine the function of histamine in the brain are considered together with the evidence linking histamine specifically with the hypothalamus. The distribution of histamine and the enzymes responsible for its synthesis and metabolism is consistent with there being both mast cells and histaminergic nerve terminals within the hypothalamus. Iontophoresis, mepyramine binding and histamine-stimulated adenylate cyclase studies suggest that both histamine H1- and H2- receptors are present in the hypothalamus. In addition, intracerebroventricularly injected histamine receptor agonists and antagonists affect many functions associated with the hypothalamus such as cardiovascular control, food intake, body temperature control, and pituitary hormones whose release is mediated via the hypothalamus, such as corticotropin, growth hormone, thyroid stimulating hormone, prolactin, gonadotropins and vasopressin. However, only in the case of thyroliberin release, prolactin release, body fluid control and blood pressure control is there evidence yet that such effects are mediated via histamine receptors actually in the hypothalamus. The effects of enzyme inhibitors suggest endogenous histamine may be involved in the physiological control of thyroid stimulating hormone, growth hormone and blood pressure, and the effects of receptor antagonists support a role for endogenous histamine in prolactin control. Otherwise, there is little evidence for a physiological role for endogenous, as against exogenous, histamine whether it be from histaminergic terminals or mast cells. In addition, few studies have tried to distinguish possible effects on presynaptic receptors, postsynaptic receptors, hypothalamic blood vessels or the hypophyseal portal blood vessels. It is concluded that although there is good evidence now linking histamine and the hypothalamus more specific studies are required, for instance using microinjection or in vitro techniques and the more specific chemical tools now available, to enable a clearer understanding of the physiological role of histamine in the hypothalamus.
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PMID:Histamine and the hypothalamus. 631 74

In this paper we use the published data of others as well as our own recent data to question the widespread assumption that the gene for guinea pig insulin mutated rapidly after the divergence of guinea pigs from the main line of rodent evolution. We suggest that instead guinea pigs may have two pairs of alleles, one for typical guinea pig insulin, which is expressed in its pancreatic beta cells, and the other for a more typical mammalian insulin (designated rat/pork-type insulin), which is expressed in extrapancreatic cells. Further, we suggest the possibility that both pairs of genes may be evolutionarily very ancient and highly conserved. We also review evidence that the concept of nonallelic evolution may also apply to other hormones, including vasopressin, calcitonin, and growth hormone.
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PMID:Two distinct insulins in the guinea pig: the broad relevance of these findings to evolution of peptide hormones. 634 24

Neuron-specific enolase (NSE) was localized, using the immunoperoxidase technique, in the cytoplasm of the five adenohypophyseal hormone-secreting cell types, and in nerve fibers of the pars nervosa of the human pituitary. Crooke's hyaline material was negative. Neuron-specific enolase was found in all pituitary adenoma types; there was no correlation between degree of granularity or differentiation of tumor cells and intensity of NSE immunopositivity. One hypothalamic hamartoma was positive for NSE; a craniopharyngioma and a neurohypophyseal granular cell tumor were not. Neuron-specific enolase was present in peptide hormone-producing endocrine cells outside the pituitary and in their tumors; the majority of other tumors were negative for NSE, although one breast carcinoma, one ovarian cystadenocarcinoma, and one lymphoma were positive for NSE. In control studies, absorption of NSE antisera with growth hormone abolished immunoreactivity; there was no immunologic cross-reaction demonstrable by radioimmunoassay.
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PMID:Immunohistochemical localization of neuron-specific enolase in the human hypophysis and pituitary adenomas. 636 13

The hormonal responses to insulin-induced hypoglycemia were studied in 15 abstinent alcoholics with varying degrees of central and peripheral nerve damage and in six normal controls. Blood samples were taken at intervals after the injection of soluble insulin (0.1 U/kg of body weight). Growth hormone responses were significantly depressed (p less than 0.05) in nine alcoholics with severe central nerve damage (Korsakoff's psychosis) as compared to other alcoholic subjects. The alcoholic subjects with Korsakoff's psychosis also showed significant depression (p less than 0.01) of glucose recovery from hypoglycemia as compared with controls. However, responses of vasopressin, cortisol, and catecholamines (epinephrine and norepinephrine) were generally normal in the Korsakoff patients. Our results do not support previous suggestions that impairment of memory in alcoholism may be related to altered vasopressin secretion, even though the reduced growth hormone secretion in brain-damaged alcoholics does indicate some hypothalamic-pituitary dysfunction.
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PMID:Growth hormone, vasopressin, cortisol, and catecholamine responses to insulin hypoglycemia in alcoholics. 637 19


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