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 effects of cortisol, its steric analog 11-epicortisol, and lysine vasopressin (LVP) on DNA and RNA synthesis in isolated adrenocorticotropic hormone-secreting human pituitary tumor cells obtained by transsphenoidal surgery were studied using [3H]thymidine incorporation in DNA and [3H]uridine in RNA. Cortisol suppressed RNA and, to a greater extent, DNA synthesis in these cells. This could explain the slow growth of pituitary tumors in patients with Cushing's disease and the rapid growth of Nelson's pituitary tumors after bilateral adrenalectomy. 11-Epicortisol also suppressed RNA synthesis, but it had a stimulatory effect on DNA synthesis, which indicates a high specificity of glucocorticoid receptors. When applied together with cortisol, 11-epicortisol antagonized the suppressive effects of cortisol on DNA synthesis. Although LVP stimulated RNA synthesis, it suppressed DNA synthesis in most of the tumor cells.
Steroids 1990 Mar
PMID:The effects of cortisol, 11-epicortisol, and lysine vasopressin on DNA and RNA synthesis in isolated human adrenocorticotropic hormone-secreting pituitary tumor cells. 215 95

A 32-year-old woman was bedridden for a year because of chronic pain and headaches. She had insomnia, depression, suicidal thoughts and a severe chemical allergy. She had been on steroid therapy for two years and became Cushingoid with striae in the arm pits, groins and abdomen. However, she had no hypertension, nor the buffalo fat and hirsutism. She was very edematous, with a weight gain from 112 to 180 lbs. The fluid retention did not conform to the syndrome of inappropriate antidiuretic hormone. Studies revealed abnormal scalp EEG discharges and high-voltage seizure discharges in the posterior thalamus. Electrothalamic stimulation suppressed the thalamic discharges and relieved the patient's pelvic pain and headaches. After one month of several thalamic stimulations per day, she was able to get out of bed and ambulate. In addition, the patient no longer was edematous and was tolerating perfumes and floor detergents. Steroids were progressively reduced without complications of withdrawal. She went from a completely steroid dependent state to independent during the first 1-1/2 yrs of thalamic stimulation. With continued thalamic stimulation she has done well for 8-1/2 yrs, weighs 112 lbs, keeps house and drives a car. It's speculated the illness is a chronic pain multiple syndrome predominantly due to mesothalamic discharges and body infirmities. The mesothalamic discharge implicated neural networks, which represent biologic systems, i.e. pain, sleep, fluid retention, etc. Therapeutic stimulation attenuates the discharges and the neural networks return to their normal set points of homeostasis.
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PMID:Mesothalamic discharge in a chronic pain, allergy and fluid retention syndrome (case report). 766 2

The effect of human chorionic gonadotropin (hCG) on intact Leydig cell phospholipid methylation was studied. Hormonal stimulation of rat Leydig cells increased the incorporation of [methyl-3H]methionine into phospholipids threefold. This effect was observed after 10 minutes of incubation time and was time and dose dependent with a maximal stimulation at 67 ng/ml of hCG. In the presence of hCG, 3H-labeled methyl groups were preferentially incorporated into phosphatidyl-N-monomethylethanolamine. This effect of hCG was not reproduced by dibutyryl cyclic adenosine monophosphate (cAMP), cholera toxin, or forskolin. Purified hCG beta subunit but not hCG alpha subunit had stimulatory activity on Leydig cell phospholipid methylation. We conclude that luteinizing hormone (LH)/hCG stimulates specifically Leydig cell phospholipid methylation, because LH-releasing hormone or [Arg8]-vasopressin did not modify these reactions. We postulate that these reactions are occurring at a cellular level that involves hormone-receptor interaction. It is also suggested that this biological response involves hCG beta subunit receptor interaction and does not require cAMP synthesis.
Steroids 1993 Jul
PMID:Human chorionic gonadotropin and free beta subunits stimulate phospholipid methylation in intact rat Leydig cells. 769 25

Although the stimulations of renal hypertrophy and renal erythropoietin production have been well-known androgen effects in the kidney, recent investigative progresses are further providing good evidences for androgen-regulated gene productions of key enzymes or local hormone substrates important to renal cell metabolisms and tubular functions in mouse or rat proximal tubules, respectively. It has been also reported that testosterone restores vasopressin receptors in medullary collecting ducts of the ageing rat and improves a urinary concentrating ability. Therefore in the present study we examined a metabolic pathway of androgens in cultured rat renal IMCD cells, which finally determine a urinary composition and volume. IMCD cells cultured from kidneys of male Wistar rats weighing about 200 g were incubated with serum-free culture media containing 4 nM [3H] testosterone or [3H] androstenedione for 2-48 h. Radioactive compounds in incubation media were then separated by reverse-phase high-pressure liquid chromatography (HPLC) and identified mainly on the basis of comparison of retention times of standard materials on HPLC. The main metabolites identified in testosterone or androstenedione incubation experiment were 5 alpha-dihydrotestosterone or 5 alpha-androstanedione, respectively. 5 alpha-Reductase inhibitor, MK 906, effectively inhibited the formations of these Ring A reduced metabolites. These results may suggest that rat renal IMCD cells possess 5 alpha-reductase activity, thereby converting androgens into their biologically active forms in vivo.
Steroids 1998 Feb
PMID:Androgen metabolism in cultured rat renal inner medullary collecting duct (IMCD) cells. 951 21

Steroid, amine and peptide hormones affect the peripheral vestibular system. Vasopressin hypersensitivity of the endolymphatic sac may be implicated in the pathogenesis of Meniere's disease. Specific vasopressin antagonists will help define the role of vasopressin in Meniere's disease. The modulation of central vestibular pathways by neuroactive steroids may involve effects on gamma-aminobutyric acid-ergic and glutaminergic pathways. The vestibular nuclei also express enzymes that are important in the synthesis of steroids and the modulation of their activity. Steroids mediate both facilitatory and deleterious effects of stress on vestibular compensation. The quality and quantity of stressor that determines the pattern of hormonal output, may be important. Clinical observation suggests that episodic ataxia type 2, a P/Q calcium channelopathy, may be phenotypically modulated by endocrine fluctuations. Steroid hormones may affect the episodic ataxia type 2 phenotype by modulation of voltage-gated calcium channel activity via second messenger systems and ion channel subunit expression. Despite evidence to support the link, the role of the endocrine system in vestibular function and disease is as yet virtually unexplored.
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PMID:The endocrine system, vertigo and balance. 1117 14

Steroids and peptides mediate a diverse array of animal social behaviors. Human research is restricted by technical-ethical limitations, and models of the neuroendocrine regulation of social-emotional behavior are therefore mainly limited to non-human species, often under the assumption that human social-emotional behavior is emancipated from hormonal control. Development of acute hormone administration procedures in human research, together with the advent of novel non-invasive neuroimaging techniques, have opened up opportunities to systematically study the neuroendocrinology of human social-emotional behavior. Here, we review all placebo-controlled single hormone administration studies addressing human social-emotional behavior, involving the steroids testosterone and estradiol, and the peptides oxytocin and vasopressin. These studies demonstrate substantial hormonal control over human social-emotional behavior and give insights into the underlying neural mechanisms. Finally, we propose a theoretical model that synthesizes detailed knowledge of the neuroendocrinology of social-emotional behavior in animals with the recently gained data from humans described in our review.
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PMID:Acute effects of steroid hormones and neuropeptides on human social-emotional behavior: a review of single administration studies. 2125 59

The complex interaction between hypothalamus, pituitary and adrenal glands is a key component of the neuroendocrine stress response. The major stress hormones--glucocorticoids--have both central and peripheral effects. Among the factors regulating their availability to target tissues are levels of corticosteroid-binding globulin, as the major transport protein for glucocorticoids in systemic circulation. Our recent findings demonstrated expression of corticosteroid-binding globulin in various brain regions and in different cell populations (neurons and glial cells). We showed at the cellular level the presence of corticosteroid-binding globulin in the human hypothalamus, where it was co-localized with the classical neurohypophyseal neurohormones--vasopressin and oxytocin. For the first time we demonstrated in mouse that the same gene encodes brain and liver corticosteroid-binding globulin. The full-length sequencing of hypothalamic corticosteroid-binding globulin revealed a full homology with liver corticosteroid-binding globulin cDNA. Thus, we confirmed that corticosteroid-binding globulin mRNA is produced locally within various cerebral regions and thus not transported from blood. However, the amounts of mRNA encoding corticosteroid-binding globulin are in liver about 200 times higher than in brain. The wide distribution of corticosteroid-binding globulin, distinct from the localization of glucocorticoid receptors, observed in our comparative study in rodents, led us to propose two possibilities: (1) corticosteroid-binding globulin is made in certain neurons to deliver glucocorticoids into the cell and within the cell in the absence of cytoplasmic glucocorticoid receptors or (2) is internalized into neurons specifically to deliver glucocorticoids to classical glucocorticoid receptors. Brain corticosteroid-binding globulin may be involved in the response to changing systemic glucocorticoid levels either additionally to known nuclear and membrane corticosteroid receptors or in glucocorticoid responsive brain regions devoid of these receptors. Clearly the multiple locations of corticosteroid-binding globulin within the central nervous system of humans and rodents imply multiple functional properties in normal and/or pathological conditions, which are yet to be determined. Most likely, the importance of brain corticosteroid-binding globulin exceeds the function of a mere steroid transporter.
Steroids 2014 Mar
PMID:Adrenal steroids in the brain: role of the intrinsic expression of corticosteroid-binding globulin (CBG) in the stress response. 2424 37

The hypothalamo-neurohypophyseal system plays a key role in maintaining homeostasis and in regulation of numerous adaptive reactions, e.g., endocrine stress response. Nonapeptides vasopressin and oxytocin are the major hormones of this system. They are synthesized by magnocellular neurons of the paraventricular and supraoptic hypothalamic nuclei. Magnocellular vasopressin is known to be one of the main physiological regulators of water-electrolyte balance. Its importance for control of the hypothalamo-pituitary-adrenal axis has been widely described. Magnocellular oxytocin is secreted predominantly during lactation and parturition. The complex actions of oxytocin within the brain include control of reproductive behavior and its involvement in central stress response to different stimuli. It's neuroendocrine basis is activation of the hypothalamo-pituitary-adrenal axis: corticotropin-releasing hormone is synthesized in parvocellular neurons of the paraventricular hypothalamic nuclei. The transitory coexpression of vasopressin in these cells upon stress has been described. Glucocorticoids, the end products of the hypothalamo-pituitary-adrenal axis have both central and peripheral actions. Their availability to target tissues is mainly dependent on systemic levels of corticosteroid-binding globulin. Intrinsic expression of this protein in different brain regions in neurons and glial cells has been recently demonstrated. Regulation of the hypothalamo-pituitary-adrenal axis and hypothalamo-neurohypophyseal system is highly complex. The role of both systems in the pathogenesis of various chronic ailments in humans has extensively been studied. Their disturbed functioning seems to be linked to various psychiatric, autoimmune and cardiovascular pathologies.
Steroids 2016 07
PMID:Magnocellular hypothalamic system and its interaction with the hypothalamo-pituitary-adrenal axis. 2682 26

Steroid-binding globulins (SBGs) such as sex hormone binding globulin, corticosteroid binding globulin, and vitamin-D binding protein are receiving increasing notice as being actively involved in steroid actions. This paper reviews data of all three of these SBGs, focusing on their presence and possible activity in the brain and nose. We have found all three proteins in the brain in limbic areas such as the paraventricular (PVN) and supraoptic nuclei (SON) as well as other areas of the hypothalamus, hippocampus, and medial preoptic area. There is also evidence that all three are made in the PVN and SON, in conjunction with the neuropeptides oxytocin and vasopressin. The localization of these three SBGs is more variable within areas of the main olfactory area and the vomeronasal organ. However, all three are found in the mucus of these areas, suggesting that one of their functions is to sequester aerosol steroids, such as pheromones, and deliver them to sensory cells and then to deeper sensory areas. In this manuscript, we present multiple models of SBG action including: A) SBG binding to a membrane receptor, B) this SBG receptor being associated with a larger protein complex including cytoplasmic steroid receptors, C) when the SBGs binds to their SBG receptors, second messengers within the cells respond, D) after SBG binding to its receptor, it releases its associated steroid into the membrane's lipid bilayer, from which it gains access into the cell only when bound by an internal protein, E) the SBG, possibly with its bound SBG receptor, is internalized into the cell from which it can gain access to numerous organelles and possibly the cell's nucleus or F) associate with intracellular steroid receptors, G) SBGs produced in target cells are released from those cells upon specific stimulation, and H) according to the Free Steroid Hypothesis steroids released from the extracellular SBG passively diffuse across the plasma membrane of the cell. These models move the area of steroid endocrinology forward by providing important paths of steroid activity within many steroid target cells.
Steroids 2019 02
PMID:Three steroid-binding globulins, their localization in the brain and nose, and what they might be doing there. 2924 92