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)

This review discusses the possible interrelationships between adrenal steroid hormones and the metabolic syndrome. Abnormal regulation of the hypothalamic-pituitary-adrenal axis has been proposed. Studies in the United Kingdom associated the metabolic syndrome with low birth weight and hyperactivity of the entire axis. In Italy, increased pituitary responsiveness to stimulation with vasopressin and corticotrophin-releasing hormone was demonstrated in women with central obesity. Swedish researchers have reported that increased stress responses of the axis correlated with a less variable but decreased cortisol level. An allele of the glucocorticoid receptor was also associated with various components of the metabolic syndrome. Evidence also suggests that central obesity is associated with an increased peripheral conversion of cortisol to cortisone and subsequent feedback stimulation of the axis. On the other hand, central fat may have an increased local metabolism in the direction of cortisol. Roles for dehydroepiandrosterone and aldosterone in the syndrome have also been proposed.
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PMID:The adrenal and the metabolic syndrome. 1127 91

The paraventricular nucleus of the hypothalamus (PVN) is a complex effector structure that initiates endocrine and autonomic responses to stress. It receives inputs from visceral receptors, circulating hormones such as angiotensin II, and limbic circuits and contains neurons that release vasopressin, activate the adrenocortical axis, and activate preganglionic sympathetic or parasympathetic outflows. The neurochemical control of the different subgroups of PVN neurons is complex. The PVN has been implicated in the pathophysiology of congestive heart failure and the metabolic syndrome.
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PMID:Paraventricular nucleus, stress response, and cardiovascular disease. 1603 78

Impaired insulin-mediated vasodilation has been implicated in hypertension that is associated with the metabolic syndrome. The aim of this study was to determine whether an abnormality in membrane fatty acid composition was related to a weakening of insulin's inhibitory effect on agonist-stimulated intracellular free calcium elevation. Mild to moderate hypertensive patients (n = 27) and normotensive controls (n = 11) were studied. Hypertensive patients were divided into normoinsulinemic patients (n = 14) and hyperinsulinemic patients (n = 13) according to the area under the curve of plasma insulin concentrations during a 75-g oral glucose tolerance test. Nonstimulated and arginine-vasopressin (AVP) (1 micromol/l)-stimulated intraplatelet free calcium concentrations (p[Ca(2+)](i)) were measured with or without insulin (100 microU/ml) preincubation. Platelet membrane fatty acid composition, intraerythrocyte sodium content, and the ouabain-sensitive sodium efflux rate constant (K (os)) of erythrocytes were also determined. Insulin preincubation reduced AVP-stimulated p[Ca(2+)](i) elevation in both normotensive controls and hypertensive patients. The inhibitory effect of insulin on AVP-stimulated elevation of p[Ca(2+)](i) (%Inhibition) was significantly (P < 0.05) blunted in hyperinsulinemic hypertensive patients (9.7% +/- 2.4%) as compared to normoinsulinemic hypertensive patients (17.4% +/- 2.7%) and normotensive controls (16.9% +/- 1.7%). In hypertensive patients, the %Inhibition was correlated negatively with saturated fatty acids (SFA) (r = -0.51, P < 0.05) and systolic blood pressure (r = -0.44, P < 0.05), and correlated positively with membrane polyunsaturated fatty acids (PUFA) (r = 0.53, P < 0.01) and K (os) (r = 0.53, P < 0.005). Multiple regression analysis showed that SFA, PUFA, and K (os) were the significant variables for %Inhibition. These findings indicate that an increase in SFA and a decrease in PUFA may cause insulin insensitivity in cellular calcium and sodium handling in hypertension with hyperinsulinemia.
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PMID:Inhibitory effect of insulin on vasopressin-induced intracellular calcium response is blunted in hyperinsulinemic hypertensive patients: role of membrane fatty acid composition. 1686 95

Non-glucocorticoid inhibitors of the HPA-system are of utmost interest in the treatment of diseases with impaired regulation of this system, like the metabolic syndrome and depression. In rats, a fragment of the thyreotropin-releasing hormone (TRH) preprohormone, preproTRH((178-199)), has been demonstrated to inhibit basal and stimulated secretion of cortisol. Our pilot study aimed to explore the first time similar effects of the homologue peptide preproTRH((158-183)) in healthy humans. In a double-blind within-subject comparison, eight healthy young men were infused intravenously with placebo and preproTRH((158-183)) at varying doses of 5, 10, 25 and 50 mg/kg of body weight. After 15 min of infusion a corticotropin-releasing hormone (CRH)/vasopressin-test was performed. Plasma concentrations of pituitary hormones and free thyroxine, blood pressure, heart rate and feelings of activation and mood were assessed repeatedly at close intervals. Individual hormone profiles and collapsed data across all doses did not reveal any effects of preproTRH((158-183)) on HPA-activity, although it increased TSH and fT4, stimulated the release of GH and increased systolic blood pressure in the course of the experiment (p<0.05, for all effects). Self-reports indicated enhanced feelings of activation and general well-being following preproTRH (p<0.05). Our data exclude a substantial inhibitory effect of preproTRH((158-183)) on HPA secretory activity and, thus, contrast with findings in rats. In humans, the peptide appears to even exert an albeit weak stimulatory effect on autonomic stress systems as indicated by increased cardiovascular activity in combination with enhanced subjective arousal.
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PMID:PreproTRH(158-183) fails to affect pituitary-adrenal response to CRH/vasopressin in man: a pilot study. 1748 75

The article critically reviews selected, clinically significant, adverse endocrine and metabolic effects associated with psychotropic drug treatments, including hyperprolactinaemia, hyponatraemia, diabetes insipidus, hypothyroidism, hyperparathyroidism, sexual dysfunction and virilization, weight loss, weight gain and metabolic syndrome (type 2 diabetes mellitus, dyslipidaemia and hypertension). Such effects are prevalent and complex, but can be managed clinically when recognized. They encourage continued critical assessment of benefits versus risks of psychotropic drugs and underscore the importance of close coordination of psychiatric and general medical care to improve long-term health of psychiatric patients. Options for management of hyperprolactinaemia include lowering doses, switching to agents such as aripiprazole, clozapine or quetiapine, managing associated osteoporosis, carefully considering the use of dopamine receptor agonists and ruling out stress, oral contraceptive use and hypothyroidism as contributing factors. Disorders of water homeostasis may include syndrome of inappropriate antidiuretic hormone (SIADH), managed by water restriction or slow replacement by hypertonic saline along with drug discontinuation. Safe management of diabetes insipidus, commonly associated with lithium, involves switching mood stabilizer and consideration of potassium-sparing diuretics. Clinical hypothyroidism may be a more useful marker than absolute cut-offs of hormone values, and may be associated with quetiapine, antidepressant and lithium use, and managed by thyroxine replacement. Hyper-parathyroidism requires comprehensive medical evaluation for occult tumours. Hypocalcaemia, along with multiple other psychiatric and medical causes, may result in decreased bone density and require evaluation and management. Strategies for reducing sexual dysfunction with psychotropics remain largely unsatisfactory. Finally, management strategies for obesity and metabolic syndrome are reviewed in light of the recent expert guidelines, including risk assessment and treatments, such as monoamine transport inhibitors, anticonvulsants and cannabinoid receptor antagonists, as well as lifestyle changes.
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PMID:Adverse endocrine and metabolic effects of psychotropic drugs: selective clinical review. 1995 39

In spite of significant progress in pharmacotherapy the incidence of newly diagnosed cases of cardiovascular diseases and cardiovascular morbidity is alarmingly high. Treatment of hypertension or heart failure still remains a serious challenge. Continuous attempts are made to identify the mechanisms that decide about susceptibility to pathogenic factors, and to determine effectiveness of a specific therapeutic approach. Coincidence of cardiovascular diseases with metabolic disorders and obesity has initiated intensive research for their common background. In the recent years increasing attention has been drawn to disproportionately greater number of depressive disorders and susceptibility to stress in patients with coronary artery disease. An opposite relationship, i.e. a greater number of sudden cardiovascular complications in patients with depression, has been also postulated. Progress in functional neuroanatomy and neurochemistry provided new information about the neural network responsible for regulation of cardiovascular functions, metabolism and emotionality in health and under pathological conditions. In this review we will focus on the role of neuromodulators and neurotransmitters engaged in regulation of the cardiovascular system, neuroendocrine and metabolic functions in health and in pathogenesis of cardiovascular diseases and obesity. Among them are classical neurotransmitters (epinephrine and norepinephrine, serotonin, GABA), classical (CRH, vasopressin, neuropeptide Y) and newly discovered (orexins, apelin, leptin IL-1beta, TNF-alpha, ghrelin) neuropeptides, gasotransmitters, eicozanoids, endocannabinoids, and some other compounds involved in regulation of neuroendocrine, sympatho-adrenal and parasympathetic nervous systems. Special attention is drawn to those factors which play a role in immunology and inflammatory processes. Interaction between various neurotransmitter/neuromodulatory systems which may be involved in integration of metabolic and cardiovascular functions is analyzed. The survey gives evidence for significant disturbances in release or action of the same mediators in hypertension heart failure, obesity, diabetes mellitus, metabolic syndrome, starvation, chronic stress, depression and other psychiatric disorders. With regard to the pathogenic background of the cardiovascular diseases especially valuable are the studies showing inappropriate function of angiotensin peptides, vasopressin, CRH, apelin, cytokines and orexins in chronic stress, cardiovascular and metabolic diseases. The studies surveyed in this review suggest that multiple brain mechanisms interact together sharing the same neural circuits responsible for adjustment of function of the cardiovascular system and metabolism to current needs.
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PMID:Brain and cardiovascular diseases: common neurogenic background of cardiovascular, metabolic and inflammatory diseases. 2108 94

Addition of mineralocorticoid receptor (MR) antagonists to standard therapy for heart failure, kidney disease, metabolic syndrome, and diabetes is increasing steadily in response to clinical trials demonstrating clear benefits. In addition to blocking deleterious activity of MR within the heart, vessels and kidneys, MR antagonists target MR in hemodynamic regulatory centers in the brain, thereby decreasing excessive sympathetic nervous system drive, vasopressin release, abnormal baroreceptor function, and circulating and tissue pro-inflammatory cytokines. However, brain MR are also involved with cognition, memory, affect and functions yet to be determined. Understanding specific central mechanisms involved in blood pressure regulation by MR is necessary for the development of agents to target downstream events specific to central hemodynamic regulation, not only to avoid the hypokalemia caused by inhibition of renal tubular MR, but also to avoid untoward long term effects of inhibiting brain MR that are not involved in blood pressure control.
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PMID:Central regulation of blood pressure by the mineralocorticoid receptor. 2166 17

Taking into account the high prevalence of renal disease in metabolic syndrome (MS), relationship between the reduction of the renal function and severity of disorders of lipid metabolism and increased risk of cardiovascular complications, evaluation of electrolyte and nitrogen metabolism was performed for 112 patients with MS. In addition, serum levels ofaldosterone, adrenocorticotropic hormone, neutrophil gelatinase-associated lipocalin, cortisol, beta2-microglobulin, vasopressin, and level of microalbumin in urine were assessed. MS patients showed a reduction of the daily expression of the main osmotically active substance - urea, potassium, sodium and chloride. The increased production of antidiuretic hormone and related water retention, increased microalbumin excretion, indicating the development of systemic endothelial dysfunction and glomerular hyperfiltration, were detected. Reported violations are developing by type of "vicious circle": fluid retention leads to hyperfiltration, renal dysfunction exacerbates water-electrolyte disorders.
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PMID:[Water and electrolyte metabolism disturbances in patients with metabolic syndrome]. 2311 19

After several decades during which little attention was paid to vasopressin and/or urine concentration in clinical practice, interest in vasopressin has renewed with the availability of new, potent, orally active vasopressin-receptor antagonists--the vaptans--and with the results of epidemiological studies evaluating copeptin (a surrogate marker of vasopressin) in large population-based cohorts. Several experimental studies in rats and mice had previously shown that vasopressin, acting via vasopressin V2 antidiuretic receptors, contributes to the progression of chronic kidney disease; in particular, to autosomal dominant polycystic kidney disease. New epidemiological studies now suggest a role for vasopressin in the pathogenesis of diabetes mellitus and metabolic disorders via activation of hepatic V1a and/or pancreatic islet V1b receptors. The first part of this Review describes the adverse effects of vasopressin, as revealed by clinical and experimental studies in kidney diseases, hypertension, diabetes and the metabolic syndrome. The second part provides insights into vasopressin physiology and pathophysiology that may be relevant to the understanding of these adverse effects and that are linked to the excretion of concentrated nitrogen wastes and associated hyperfiltration. Collectively, the studies reviewed here suggest that more attention should be given to the vasopressin-thirst-urine concentration axis in clinical investigations and in patient care. Whether selective blockade of the different vasopressin receptors may provide therapeutic benefits beyond their present indication in hyponatraemia requires new clinical trials.
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PMID:Vasopressin: a novel target for the prevention and retardation of kidney disease? 2343 73

Elevated plasma CT-pro-vasopressin (copeptin) has been described as biomarkers for type 2 diabetes (T2D) and the metabolic syndrome (MetS), which, however, was not confirmed by all studies. Here, we analyzed the association of copeptin with T2D, MetS and MetS components in the population-based KORA F4 study. Plasma copeptin concentrations were analyzed in 1,554 study participants. We used fractional polynomial selection procedures to check for nonlinearity of the associations between copeptin and T2D and HbA1c, respectively. In logistic regression models, we investigated associations between copeptin and T2D, MetS and its components according to IDF criteria. In the fractional polynomial approach, linear models fitted best for copeptin. In multivariable adjusted models, copeptin as a continuous variable was associated with T2D and HbA1c only in men (OR = 1.38 per standard deviation, 95 % CI 1.13-1.70 for T2D). Comparing the top quartile Q4 versus Q1-3, elevated copeptin was associated with T2D (OR 2.70, 95 % CI 1.60-4.59) in men but not in women (OR 0.98, 95 % CI 0.52-1.83). Copeptin was not significantly associated with MetS, central obesity, triglycerides and reduced HDL cholesterol. A significant association with copeptin was observed for hypertension in women (OR 1.59, 95 % CI 1.08-2.33) and glucose dysfunction according to IDF criteria in men (OR 1.63, 95 % CI 1.14-2.34). In the KORA F4 study, copeptin was significantly associated with T2D only in men, whereas hypertension was associated with copeptin in women. No other components of the MetS were related to elevated copeptin.
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PMID:Plasma copeptin is associated with type 2 diabetes in men but not in women in the population-based KORA F4 study. 2501 50


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