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 author presents an account of selected important findings in endocrinology during the last year. The mediator of action of STH, IGF-I, was tested as a protein anabolic in a child with Laron's nanism. STH is about to be tested as a geriatric drug. A non-peptide vasopressin antagonist was described. Melatonin is being tested in sleep disorders. A combination of methimazol and thyroxine is more suitable for treatment of Graves-Basedow's disease than the goitrogen alone. Dermal vasoconstriction can be an indicator of the effectiveness of glucocorticoids in asthma. Significant advances were made in the sphere of the new hormone, NO: it is not only an effective vasorelaxing agent but also a neuromodulator and participates in the natural lymphocytic cytotoxicity. Marked advances were made as regards knowledge of the endogenous ligand for benzodiazepine receptors.
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PMID:[Endocrinology 1990-1991]. 180 40

This study of seventeen patients presenting to the emergency room with acute severe asthma determined levels of antidiuretic hormone in serum as well as serum electrolytes and arterial blood gases serially. There was a progressive increase in plasma ADH concentration with severe asthma and ADH levels were substantially higher in those patients with PaCO2's higher than 45 Torr. Patients treated with intravenous aminophylline had a fall in ADH levels while those treated with injectable epinephrine showed an elevation of these levels. As the asthma improved, ADH levels decreased in all patients. In this series of children, sick for not more than 24 hours, serum sodium levels were normal. However, children who have been ill for longer periods than this or who are on prolonged intravenous fluid therapy need close monitoring of serum electrolyte concentrations.
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PMID:Antidiuretic hormone in acute asthma in children: effects of medication on serum levels and clinical course. 276 25

Since the approval of lithium use in treatment of acute mania, there have been numerous clinical trials of lithium in medical and psychiatric disorders. This paper gives a brief review of the literature on lithium trials in approximately fourteen medical conditions. These are: hyperthyroidism, metabolizing thyroid cancer, syndrome of inappropriate secretion of antidiuretic hormone, premenstrual tension syndrome, anorexia nervosa, Felty's syndrome, chemotherapy-induced neutropenia, aplastic anemia, seborrheic dermatitis, eczematoid dermatitis, cyclic vomiting, diabetes mellitus and asthma. Most of the case reports cited showed the efficacy of the side effects from lithium salt in the management of the symptoms and signs of these disorders, however, well-designed and controlled studies give negative results. The positive results are reported in the group of disorders having an underlying subdromal affective syndrome such as premenstrual tension syndrome and anorexia nervosa. Other encouraging reports include the effect of lithium to induce leucocytosis in Felty's syndrome and chemotherapy-induced neutropenia.
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PMID:A review of clinical trials of lithium in medicine. 639 35

Plasma antidiuretic hormone concentrations were measured in a group of children with acute asthma and in a control group. Very high levels of antidiuretic hormone were found in the asthmatic group. There were no changes in other biochemical indices. If overproduction of antidiuretic hormone is sustained then fluid administration to children with severe acute asthma is potentially dangerous.
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PMID:Acute asthma and antidiuretic hormone secretion. 661 49

Drug loads were used to diagnose impairments of the hypothalamic-pituitary-adrenal system in 209 patients with bronchial asthma. A thyroid-releasing hormone test made in patients with moderate bronchial asthma who were taking no corticosteroids (CS) demonstrated a high level of thyroid-stimulating hormone at min 60 of the agent administration, which was indicative of decreased hypothalamic function. In 67.8% of patients, the vasopressin test was positive and suggested that the pituitary preserved its functional capacities. The decreased secretion of hydrocortisone and its active forms was observed in patients with severe bronchial asthma when CS was used in the daily dose adequate to 10-15 mg of prednisolone for 5 years. The 20-day therapy with dexamethasone demonstrated that the agent reduced the synthesis of hydrocortisone to a greater extent than that of corticosterone. The administration of depot-synacthen 24 hours later elevated the content of all hydrocortisone fractions and biologically active corticosterone. Depot-synacthen exerted an active stimulating action on the adrenal cortex.
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PMID:[Evaluation of the hormonal status of patients with bronchial asthma by using various drug doses]. 860 Oct 83

ANAESTHETICS, ENDOCRINE SYSTEM, AND STRESS: The effects of anaesthetics on the nervous system are invariably associated with endocrine reactions, which are of great importance for the general characterization of anaesthetics or anaesthetic regimens. In this context, the endocrine stress response is mainly represented by adrenaline (A), noradrenaline (NA), antidiuretic hormone/vasopressin (ADH), adrenocorticotropic hormone (ACTH), and cortisol. PHARMACOLOGICAL PROFILE AND ANAESTHETIC ACTION OF KETAMINE: The pharmacological profile of ketamine is characterized by the term "dissociative anaesthesia." At the present time, the anaesthetic action of ketamine cannot be explained by a single mechanism. Its overall action might be due to different central and peripheral factors, and stereospecific effects are obvious. ENDOCRINE RESPONSES TO RACEMIC KETAMINE AND S(+)-KETAMINE: In contrast to stereospecific differences in the anaesthetic action of racemic ketamine and S-(+)-ketamine, the endocrine reactions to the S-(+) isomer and the racemic mixture are very similar. When S(+)-ketamine is used as the sole anaesthetic, significant activation of the sympathoadrenergic system with increases in plasma levels of A and NA can be observed. This effect is mitigated by midazolam. In combination with propofol, sympathoadrenergic responsiveness is preserved without overwhelming effects. In contrast to monoanaesthesia with S(+)-ketamine, during combination with midazolam and propofol significant increases in plasma ADH levels are observed, which might be due to suppressed sympathoadrenergic reactivity. In addition, surgical stress activates the pituitary-adrenocortical system with increases in ACTH and cortisol. Effects of midazolam and propofol on this effect are similar. SYNOPSIS AND CLINICAL ASPECTS: S-(+)-ketamine as a monoanaesthetic has significant sympathomimetic properties, which are beneficial during induction of patients in shock and patients with asthma. The combination of S-(+)-ketamine and midazolam has weaker sympathomimetic and general endocrine-stimulating properties, and can be used for analgosedation in patients with cardiovascular instability and exogenous catecholamine requirements. In combination with propofol, the sympathomimetic and general endocrine-stimulating effects of S-(+)-ketamine are less pronounced because of contrasting properties of both drugs. This combination might be useful in patients with endocrine deficits and for analgosedation, when rapid recovery is necessary and negative circulatory effects should be avoided.
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PMID:[Endocrine reactions following S-(+)-ketamine]. 916 76

Corticotropin-releasing hormone (CRH) is a major regulator of the hypothalamic-pituitary-adrenal axis (HPA) and principal coordinator of the stress response. As in stress, intracerebroventricular administration of CRH suppresses the immune system indirectly, via glucocorticoid and/or sympathetic system-mediated mechanisms. Also, during inflammatory stress, the cytokines TNF alpha, IL-1, and IL-6 stimulate hypothalamic CRH and/or vasopressin secretion as a way of preventing the inflammatory reaction from overreacting. Recently, CRH receptors were described in peripheral sites of the immune system, and CRH was found to promote several immune functions in vitro. We demonstrated a direct role of CRH in the inflammatory immune process in vivo, by first studying the effect of systemic CRH immunoneutralization in an experimental model of carrageenin-induced aseptic inflammation in Spague-Dawley rats. We extended these observations to other forms of experimental inflammation, including streptococcal cell wall polysaccharide- and adjuvant-induced arthritides and peptide R16 (epitope of the interphotoreceptor retinoid-binding protein)-induced uveitis in Lewis rats. We also studied human disease states, including rheumatoid arthritis, Hashimoto thyroiditis, and ulcerative colitis. Inflamed tissues contained large amounts of IR CRH, reaching levels similar to those observed in the hypophyseal portal system. We also demonstrated the presence of CRH mRNA and CRH receptors in inflammatory cells and identified the mast cells as a major immune target for CRH. In addition to production by immune cells, the peripheral nervous system, including the postganglionic sympathetic neurons and the sensory fibers type C, appears to contribute to IR CRH production in inflammatory sites. The production of CRH from the postganglionic sympathetic neurons may be responsible for the stress-induced activation of allergic/autoimmune phenomena, such as asthma and eczema, via mast cell degranulation. Antalarmin, a novel nonpeptide CRH receptor antagonist, displaced 125I-labeled ovine CRH binding in rat pituitary, frontal cortex, and cerebellum, but not heart, consistent with antagonism at the CRHR1 receptor. In vivo antalarmin significantly inhibited CRH-stimulated ACTH release and carrageenin-induced subcutaneous inflammation in rats. Thus, antalarmin and other related compounds that antagonize CRH at the level of its own receptor have therapeutic potential in some forms of inflammation directly mediated by type 1 CRH receptors and promise to enhance our understanding of the many roles of CRH in immune/inflammatory reactions.
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PMID:Corticotropin-releasing hormone and inflammation. 962 33

A 64-year-old Japanese male was admitted to Kotoh General Hospital because of fever and cough on July, 14, 1997. Laboratory data showed hypereosinophilia (11,500/microliter) and high titer of anti-myeloperoxidase antineutrophil cytoplasmic antibody (319 EU). A physical examination revealed progressive peripheral neuropathy. He had been diagnosed as having bronchial asthma since November, 1996. Therefore, he was diagnosed as having Churg-Strauss syndrome (CSS). He was treated with methylprednisolone pulse therapy (500 mg/day for 3 days) and oral prednisolone (PSL, 60 mg/day). However, peripheral neuropathy was rapidly progressive, and echocardiogram revealed cardiac hypofunction (ejection fraction (EF); 39%). He was refereed to Akita University Hospital for further examination. On admission, laboratory data showed hyponatremia (125 mEq/l) with inappropriate secretion of antidiuretic hormone (ADH, 13.0 pg/ml). Atrial natriuretic peptide was normal (26 pg/ml). Urinary osmorality was 488 mOsm/l, and urinary sodium excretion was 86 mEq/l. Renal, adrenal, and thyroid functions were normal. From these data, his hyponatremia was caused by syndrome of inappropriate secretion of ADH (SIADH). After cyclophosphamide-pulse therapy (500 mg) and oral administration of cyclophosphamide (50 mg/day) and PSL (50 mg/day), peripheral neuropathy improved gradually, and his serum sodium returned to normal, but cardiac hypofunction continued. A possible relationship between SIADH and CSS is discussed.
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PMID:[Severe peripheral neuropathy, cardiac hypofunction, and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in a patient with Churg-Strauss syndrome]. 1061 73

Endothelins are peptide tissue hormones with a powerful vasoconstrictor effect. The most important one among them, endothelin-1, is the most powerful vasoconstrictor substance in the human organism which causes constriction of the blood vessels, in particular renal, coronary, pulmonary and cerebral arteries, bronchioles, and inhibits the secretion of atrial natriuretic factor and vasopressin. Because of these effects importance in the pathogenesis of some diseases is ascribed to it, e.g. myocardial infarction, cardiac failure, asthma bronchiale, Raynaud a syndrome, renovascular disease, cyclosporin-induced nephrotoxicity and cerebrovascular attacks. Although there is little direct evidence on the role of endothelins in arterial hypertension, some authors prove its importance at least in some of its forms, e.g. salt sensitivity, or in complications of hypertension. The results of experimental and human studies with antagonists of endothelin receptors and endothelin-converting enzyme blockers also support the role of endothelin in the pathogenesis of hypertension. The use of these antagonists in the treatment of hypertension calls however for further long-term studies.
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PMID:[Endothelins--physiology, pathophysiology and importance in arterial hypertension]. 1134 33

In recent years, transgenic mouse models have been developed to examine the underlying cellular and molecular mechanisms of lung disease and pulmonary vascular disease, such as asthma, pulmonary thromboembolic disease, and pulmonary hypertension. However, there has not been systematic characterization of the basic physiological pulmonary vascular reactivity in normal and transgenic mice. This represents an intellectual "gap", since it is important to characterize basic murine pulmonary vascular reactivity in response to various contractile and relaxant factors to which the pulmonary vasculature is exposed under physiological conditions. The present study evaluates excitation- and pharmacomechanical-contraction coupling in pulmonary arteries (PA) isolated from wild-type BALB/c mice. We demonstrate that both pharmaco- and electromechanical coupling mechanisms exist in mice PA. These arteries are also reactive to stimulation by alpha(1)-adrenergic agonists, serotonin, endothelin-1, vasopressin, and U-46619 (a thromboxane A(2) analog). We conclude that the basic vascular responsiveness of mouse PA is similar to those observed in PA of other species, including rat, pig, and human, albeit on a different scale and to varying amplitudes.
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PMID:Characterization of agonist-induced vasoconstriction in mouse pulmonary artery. 1798 12


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