Corticotropin-Releasing Activity of Lysine Vasopressin Evelyn Joyce Weber Iowa State University
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DDAVP Nasal Spray Is Provided As an Aqueous Solution for Intranasal Use
DDAVP® Nasal Spray (desmopressin acetate) Rx only DESCRIPTION DDAVP® Nasal Spray (desmopressin acetate) is a synthetic analogue of the natural pituitary hormone 8-arginine vasopressin (ADH), an antidiuretic hormone affecting renal water conservation. It is chemically defined as follows: Mol. wt. 1183.34 Empirical formula: C46H64N14O12S2•C2H4O2•3H2O 1-(3-mercaptopropionic acid)-8-D-arginine vasopressin monoacetate (salt) trihydrate. DDAVP Nasal Spray is provided as an aqueous solution for intranasal use. Each mL contains: Desmopressin acetate 0.1 mg Sodium Chloride 7.5 mg Citric acid monohydrate 1.7 mg Disodium phosphate dihydrate 3.0 mg Benzalkonium chloride solution (50%) 0.2 mg The DDAVP Nasal Spray compression pump delivers 0.1 mL (10 mcg) of DDAVP (desmopressin acetate) per spray. CLINICAL PHARMACOLOGY DDAVP contains as active substance desmopressin acetate, a synthetic analogue of the natural hormone arginine vasopressin. One mL (0.1 mg) of intranasal DDAVP has an antidiuretic activity of about 400 IU; 10 mcg of desmopressin acetate is equivalent to 40 IU. 1. The biphasic half-lives for intranasal DDAVP were 7.8 and 75.5 minutes for the fast and slow phases, compared with 2.5 and 14.5 minutes for lysine vasopressin, another form of the hormone used in this condition. As a result, intranasal DDAVP provides a prompt onset of antidiuretic action with a long duration after each administration. 1 2. The change in structure of arginine vasopressin to DDAVP has resulted in a decreased vasopressor action and decreased actions on visceral smooth muscle relative to the enhanced antidiuretic activity, so that clinically effective antidiuretic doses are usually below threshold levels for effects on vascular or visceral smooth muscle. -
Management and Treatment of Lithium-Induced Nephrogenic Diabetes Insipidus
REVIEW Management and treatment of lithium- induced nephrogenic diabetes insipidus Christopher K Finch†, Lithium carbonate is a well documented cause of nephrogenic diabetes insipidus, with as Tyson WA Brooks, many as 10 to 15% of patients taking lithium developing this condition. Clinicians have Peggy Yam & Kristi W Kelley been well aware of lithium toxicity for many years; however, the treatment of this drug- induced condition has generally been remedied by discontinuation of the medication or a †Author for correspondence Methodist University reduction in dose. For those patients unresponsive to traditional treatment measures, Hospital, Department several pharmacotherapeutic regimens have been documented as being effective for the of Pharmacy, University of management of lithium-induced diabetes insipidus including hydrochlorothiazide, Tennessee, College of Pharmacy, 1265 Union Ave., amiloride, indomethacin, desmopressin and correction of serum lithium levels. Memphis, TN 38104, USA Tel.: +1 901 516 2954 Fax: +1 901 516 8178 [email protected] Lithium carbonate is well known for its wide use associated with a mutation(s) of vasopressin in bipolar disorders due to its mood stabilizing receptors. Acquired causes are tubulointerstitial properties. It is also employed in aggression dis- disease (e.g., sickle cell disease, amyloidosis, orders, post-traumatic stress disorders, conduct obstructive uropathy), electrolyte disorders (e.g., disorders and even as adjunctive therapy in hypokalemia and hypercalcemia), pregnancy, or depression. Lithium has many well documented conditions induced by a drug (e.g., lithium, adverse effects as well as a relatively narrow ther- demeclocycline, amphotericin B and apeutic range of 0.4 to 0.8 mmol/l. Clinically vincristine) [3,4]. Lithium is the most common significant adverse effects include polyuria, mus- cause of drug-induced nephrogenic DI [5]. -
VASOPRESSIN and OXYTOCIN Molecular, Cellular, and Clinical Advances ADVANCES in EXPERIMENTAL MEDICINE and BIOLOGY
VASOPRESSIN AND OXYTOCIN Molecular, Cellular, and Clinical Advances ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY Editorial Board: NATHAN BACK, State University of New York at Buffalo IRUN R. COHEN, The Weizmann Institute of Science DAVID KRITCHEVSKY, Wistar Institute ABEL LAJTHA, N. S. Kline Institutefor Psychiatric Research RODOLFO PAOLETTI, University of Milan Recent Volumes in this Series Volume 443 ADV ANCES IN LACTOFERRIN RESEARCH Edited by Genevieve Spik, Dominique Legrand, Joel Mazurier, Annick Pierce, and Jean-Paul Perraudin Volume 444 REPRODUCTIVE TOXICOLOGY: In Vitro Germ Cell Developmental Toxicology, from Science to Social and Industrial Demand Edited by Jesus del Mazo Volume 445 MA THEMA TICAL MODELING IN EXPERIMENTAL NUTRITION Edited by Andrew J. Clifford and Hans-Georg MUlier Volume 446 MOLECULAR AND CELLULAR MECHANISMS OF NEURONAL PLASTICITY: Basic and Clinical Implications Edited by Yigal H. Ehrlich Volume 447 LIPOXYGENASES AND THEIR METABOLITES: Biological Functions Edited by Santosh Nigam and Cecil R. Pace-Asciak Volume 448 COPPER TRANSPORT AND ITS DISORDERS: Molecular aIfd Cellular Aspects Edited by Arturo Leone and Julian F. B. Mercer Volume 449 VASOPRESSIN AND OXYTOCIN: Molecular, Cellular, and Clinical Advances Edited by Harts H.Zingg, Charles W. Bourque, and Daniel G. Bichet Volume 450 ADV ANCES IN MODELING AND CONTROL OF VENTILATION Edited by Richard L. Hughson, David A. Cunningham, and James Duffin Volume 451 GENE THERAPY OF CANCER Edited by Peter Walden, Uwe Trefzer, Wolfram Sterry, and Farzin Farzaneh Volume 452 MECHANISMS OF LYMPHOCYTE ACTIVATION AND IMMUNE REGULATION VII: Molecular Determinants of Microbial Immunity Edited by Sudhir Gupta, Alan Sher, and Rafi Ahmed A Continuation Order Plan is available for this series. -
Demeclocycline in the Treatment of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone
Thorax: first published as 10.1136/thx.34.3.324 on 1 June 1979. Downloaded from Thorax, 1979, 34, 324-327 Demeclocycline in the treatment of the syndrome of inappropriate secretion of antidiuretic hormone W H PERKS, E H WALTERS,' I P TAMS, AND K PROWSE From the Department of Respiratory Physiology, City General Hospital, Stoke-on-Trent, Staffordshire, UK ABSTRACT Fourteen patients with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) have been treated with demethylchlortetracycline (demeclocycline) 1200 mg daily. In 12 patients the underlying lesion was malignant. The serum sodium returned to normal (> 135 mmol/l) in all patients after a mean of 8-6 days (SD+5-3 days). Blood urea rose significantly from the pretreatment level of 4-2±2-3 mmol/l to 10-1±5-1 mmol/l at ten days (p<0 001). The average maximum blood urea was 13-4-6-8 mmol/l. In four patients the urea rose above 20 mmol/l, and in two of these demecyocycline was discontinued because of this rise. The azotaemia could be attributed to a combination of increased urea production and a mild specific drug-induced nephrotoxicity. Discontinuation of demeclocycline in six patients led to a fall in serum sodium, in one case precipitously, and return of the urea towards normal levels. Demeclocycline appears therefore to be an effective maintenance treatment of SIADH, and the azotaemia that occurs is reversible and probably dose dependent. The syndrome of inappropriate secretion of anti- Methods http://thorax.bmj.com/ diuretic hormone (SIADH) has become increas- ingly recognised as a treatable cause of stupor and Fourteen patients with a diagnosis of SIADH confusion in patients with a wide variety of based on the criteria of De Troyer and Demanet diseases (De Troyer and Demanet, 1976). -
Hypernatremia: 2 Months Back When He Had Progressive Decrease in Vision (Right > Left)
Correspondence to increased intrathoracic pressure and central radiologist regarding vascular injury when there is venous pressure, decreased venous return from the refractory hypotension so that necessary steps can be brain and increased ICP[4] taken to identify and treat iatrogenic complications that • Patients with aneurysmal SAH have disturbed might compound the pre‑existing morbidity. autoregulation of cerebral blood flow. Hence, intraoperative hypotension of any cause has an REFERENCES adverse effect on the outcome of SAH[5,6] • Patients with poor grade SAH (Fischer III/IV) and 1. Young WL, Pile-Spellman J. Anesthetic considerations for interventional Neuroradiolgy (Review). Anesthesiology angiographic evidence of vasospasm which our 1994;80:427-56. patient had, are at risk for cerebral hypoperfusion 2. Varma MK, Price K, Jayakrishnan V, Manickam B, Kessell G. because of impaired cerebral autoregulation and Anaesthetic considerations for interventional neuroradiology. thus intraoperative hypotension and cerebral Br J Anaesth 2007;99:75-85. [6,7] 3. Kent KC, Moscucci M, Mansour KA, Dimattia S, Gallagher S, hypoperfusion compounds the poor outcome Kuntz R, et al. Retroperitoneal hematoma after cardiac • Blood loss leading to severe anaemia (Hb 3.8 g%) catheterization: Prevalence, risk factors, and optimal during the procedure might have lead to decreased management. J Vasc Surg 1994;20:905-10. oxygen‑carrying capacity of blood and further 4. De Laet I, Citerio G, Malbrain ML. The influence of exacerbate the hypoxic injury to brain. intraabdominal hypertension on the central nervous system: Current insights and clinical recommendations, is it all in the Thus a combination of age, poor grade SAH, diffuse head? Acta Clin Belg Suppl 2007;1:89-97. -
Structural and Functional Evolution of the Vasopressin/Oxytocin Superfamily
The Journal of Neuroscience, September 1995, 15(g): 5989-5998 Structural and Functional Evolution of the Vasopressin/Oxytocin Superfamily: Vasopressin-Related Conopressin Is the Only Member Present in Lymnaea, and Is Involved in the Control of Sexual Behavior R. E. Van Kesteren,’ A. B. Smit,’ R. P. J. De Lange,’ K. S. Kits,’ F. A. Van Golen,’ R. C. Van Der Schors,’ N. D. De With,’ J. F. Burke,* and W. P. M. Geraertsl ‘Graduate School Neurosciences Amsterdam, Institute of Neurosciences, Faculty of Biology, Department of Experimental Zoology, Vrije Universiteit, Amsterdam, The Netherlands and *Sussex Centre for Neuroscience, School of Biological Sciences, University of Sussex, Brighton, United Kingdom It has been suggested that the gene duplication that led to Vasopressin and oxytocin are nonapeptides that are present in the formation of the vasopressin/oxytocin two-gene family all placental mammals. Although similar in structure, they serve occurred early during vertebrate evolution. However, the different functions (Ramsay, 1983). Vasopressin has anti-diuretic existence of both vasopressin- and oxytocin-related pep- activities and is involved in hydromineral regulation, whereas tides in invertebrates suggests that this duplication may oxytocin has uterotonic and milk-ejection activities and regulates have occurred much earlier, although there is no evidence aspects of reproductive behavior. Peptides related to both vaso- for the co-occurrence of vasopressin- and oxytocin-related pressin and oxytocin are present in all vertebrate classes, except peptides in the same invertebrate species. We report here the cyclostomes, which have only the vasopressin-related pep- that in Lymnaea only the vasopressin-related peptide Lys- tide vasotocin (reviewed by Acher, 1993). -
Estonian Statistics on Medicines 2013 1/44
Estonian Statistics on Medicines 2013 DDD/1000/ ATC code ATC group / INN (rout of admin.) Quantity sold Unit DDD Unit day A ALIMENTARY TRACT AND METABOLISM 146,8152 A01 STOMATOLOGICAL PREPARATIONS 0,0760 A01A STOMATOLOGICAL PREPARATIONS 0,0760 A01AB Antiinfectives and antiseptics for local oral treatment 0,0760 A01AB09 Miconazole(O) 7139,2 g 0,2 g 0,0760 A01AB12 Hexetidine(O) 1541120 ml A01AB81 Neomycin+Benzocaine(C) 23900 pieces A01AC Corticosteroids for local oral treatment A01AC81 Dexamethasone+Thymol(dental) 2639 ml A01AD Other agents for local oral treatment A01AD80 Lidocaine+Cetylpyridinium chloride(gingival) 179340 g A01AD81 Lidocaine+Cetrimide(O) 23565 g A01AD82 Choline salicylate(O) 824240 pieces A01AD83 Lidocaine+Chamomille extract(O) 317140 g A01AD86 Lidocaine+Eugenol(gingival) 1128 g A02 DRUGS FOR ACID RELATED DISORDERS 35,6598 A02A ANTACIDS 0,9596 Combinations and complexes of aluminium, calcium and A02AD 0,9596 magnesium compounds A02AD81 Aluminium hydroxide+Magnesium hydroxide(O) 591680 pieces 10 pieces 0,1261 A02AD81 Aluminium hydroxide+Magnesium hydroxide(O) 1998558 ml 50 ml 0,0852 A02AD82 Aluminium aminoacetate+Magnesium oxide(O) 463540 pieces 10 pieces 0,0988 A02AD83 Calcium carbonate+Magnesium carbonate(O) 3049560 pieces 10 pieces 0,6497 A02AF Antacids with antiflatulents Aluminium hydroxide+Magnesium A02AF80 1000790 ml hydroxide+Simeticone(O) DRUGS FOR PEPTIC ULCER AND GASTRO- A02B 34,7001 OESOPHAGEAL REFLUX DISEASE (GORD) A02BA H2-receptor antagonists 3,5364 A02BA02 Ranitidine(O) 494352,3 g 0,3 g 3,5106 A02BA02 Ranitidine(P) -
Effect of Intravenous Treatment with the Oxytocin Antagonist Atosiban on Circulating Progesterone in the Ewe
Graduate Theses, Dissertations, and Problem Reports 2011 Effect of Intravenous Treatment with the Oxytocin Antagonist Atosiban on Circulating Progesterone in the Ewe Todd M. Ramboldt West Virginia University Follow this and additional works at: https://researchrepository.wvu.edu/etd Recommended Citation Ramboldt, Todd M., "Effect of Intravenous Treatment with the Oxytocin Antagonist Atosiban on Circulating Progesterone in the Ewe" (2011). Graduate Theses, Dissertations, and Problem Reports. 3323. https://researchrepository.wvu.edu/etd/3323 This Thesis is protected by copyright and/or related rights. It has been brought to you by the The Research Repository @ WVU with permission from the rights-holder(s). You are free to use this Thesis in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you must obtain permission from the rights-holder(s) directly, unless additional rights are indicated by a Creative Commons license in the record and/ or on the work itself. This Thesis has been accepted for inclusion in WVU Graduate Theses, Dissertations, and Problem Reports collection by an authorized administrator of The Research Repository @ WVU. For more information, please contact [email protected]. Effect of Intravenous Treatment with the Oxytocin Antagonist Atosiban on Circulating Progesterone in the Ewe Todd M. Ramboldt Thesis submitted to the Davis College of Agriculture, Natural Resources and Design at West Virginia University in partial fulfillment of the requirements for the degree of Master of Science in Reproductive Physiology E. Keith Inskeep, Ph.D., Chair Robert A. Dailey, Ph.D. Jorge A. Flores, Ph.D. Faculty of Reproductive Physiology Morgantown, West Virginia 2011 Keywords: Corpus Luteum, Oxytocin, Atosiban, Progesterone, Sheep ABSTRACT Effect of Intravenous Treatment with the Oxytocin Antagonist Atosiban on Circulating Progesterone in the Ewe Todd M. -
Different Localization and Regulation of Two Types of Vasopressin Receptor
Different localization and regulation of two types of vasopressin receptor messenger RNA in microdissected rat nephron segments using reverse transcription polymerase chain reaction. Y Terada, … , T Yang, F Marumo J Clin Invest. 1993;92(5):2339-2345. https://doi.org/10.1172/JCI116838. Research Article Recent studies have revealed that arginine vasopressin (AVP) has at least two types of receptors in the kidney: V1a receptor and V2 receptor. In this study, microlocalization of mRNA coding for V1a and V2 receptors was carried out in the rat kidney using a reverse transcription and polymerase chain reaction. Large signals for V1a receptor PCR product were detected in the glomerulus, initial cortical collecting duct, cortical collecting duct, outer medullary collecting duct, inner medullary collecting duct, and arcuate artery. Small but detectable signals were found in proximal convoluted and straight tubules, inner medullary thin limbs, and medullary thick ascending limbs. Large signals for V2 receptor mRNA were detected in the cortical collecting duct, outer medullary collecting duct, and inner medullary collecting duct. Small signals for V2 receptor were found in the inner medullary thick limbs, medullary thick ascending limbs, and initial cortical collecting duct. Next, we investigated V1a and V2 receptor mRNA regulation in the dehydrated state. During a 72-h water restriction state, the plasma AVP level increased and V2 receptor mRNA decreased in collecting ducts. In contrast, V1a receptor mRNA did not change significantly. Thus, the -
Vasopressin and Oxytocin in Control of the Cardiovascular System
Send Orders of Reprints at [email protected] 218 Current Neuropharmacology, 2013, 11, 218-230 Vasopressin and Oxytocin in Control of the Cardiovascular System Nina Japundi-igon* Professor of Basic and Clinical Pharmacology and Toxicology, University of Belgrade School of Medicine, Institute of Pharmacology, Clinical Pharmacology and Toxicology, Dr Subotica 1, Belgrade, Republic of Serbia Abstract: Vasopressin (VP) and oxytocin (OT) are mainly synthesized in the magnocellular neurons of the paraventricular (PVN) and supraoptic nucleus (SON) of the hypothalamus. Axons from the magnocellular part of the PVN and SON project to neurohypophysis where VP and OT are released in blood to act like hormones. Axons from the parvocellular part of PVN project to extra-hypothalamic brain areas (median eminence, limbic system, brainstem and spinal cord) where VP and OT act like neurotransmitters/modulators. VP and OT act in complementary manner in cardiovascular control, both as hormones and neurotransmitters. While VP conserves water and increases circulating blood volume, OT eliminates sodium. Hyperactivity of VP neurons and quiescence of OT neurons in PVN underlie osmotic adjustment to pregnancy. In most vascular beds VP is a potent vasoconstrictor, more potent than OT, except in the umbilical artery at term. The vasoconstriction by VP and OT is mediated via V1aR. In some vascular beds, i.e. the lungs and the brain, VP and OT produce NO dependent vasodilatation. Peripherally, VP has been found to enhance the sensitivity of the baro-receptor while centrally, VP and OT increase sympathetic outflow, suppresse baro-receptor reflex and enhance respiration. Whilst VP is an important mediator of stress that triggers ACTH release, OT exhibits anti-stress properties. -
DDAVP Injection 4 Mcg/Ml Is Provided As a Sterile, Aqueous Solution for Injection
® DDAVPP Injection (desmopressin acetate) 4 mcg/mL Rx only DESCRIPTION DDAVP® Injection (desmopressin acetate) 4 mcg/mL is a synthetic analogue of the natural pituitary hormone 8-arginine vasopressin (ADH), an antidiuretic hormone affecting renal water conservation. It is chemically defined as follows: Mol. Wt. 1183.34 Empirical Formula: C46H64N14O12S2•C2H4O2•3H2O 1-(3-mercaptopropionic acid)-8-D-arginine vasopressin monoacetate (salt) trihydrate. DDAVP Injection 4 mcg/mL is provided as a sterile, aqueous solution for injection. Each mL provides: Desmopressin acetate 4.0 mcg Sodium chloride 9.0 mg Hydrochloric acid to adjust pH to 4 The 10 mL vial contains chlorobutanol as a preservative (5.0 mg/mL). CLINICAL PHARMACOLOGY DDAVP Injection 4 mcg/mL contains as active substance, desmopressin acetate, a synthetic analogue of the natural hormone arginine vasopressin. One mL (4 mcg) of DDAVP (desmopressin acetate) solution has an antidiuretic activity of about 16 IU; 1 mcg of DDAVP is equivalent to 4 IU. DDAVP has been shown to be more potent than arginine vasopressin in increasing plasma levels of factor VIII activity in patients with hemophilia and von Willebrand’s disease Type I. Dose-response studies were performed in healthy persons, using doses of 0.1 to 0.4 mcg/kg body weight, infused over a 10-minute period. Maximal dose response occurred at 0.3 to 0.4 mcg/kg. The response to DDAVP of factor VIII activity and plasminogen activator is dose-related, with maximal plasma levels of 300 to 400 percent of initial concentrations obtained after infusion of 0.4 mcg/kg body weight. -
The Structure and Function of V1b Vasopressin Receptor
The Structure and Function of V1b Vasopressin Receptors Yukie Goto A thesis submitted to the University of Birmingham for the degree of Doctor of Philosophy School of Biosciences University of Birmingham Edgbaston, Birmingham B15 2TT, United Kingdom September 2009 University of Birmingham Research Archive e-theses repository This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. Acknowledgement Firstly I would like to thank my supervisor Professor Mark Wheatley for giving me this opportunity to participate in his research, and for his support and guidance throughout my study. I would also like to thank those who have worked in his research group: in particular John for providing us with molecular models of vasopressin receptors; Alex, Mattew, Denise, Cymone and Amelia, for equipping me with the laboratory techniques required for carrying out this study; and Rachel and Richard for their companies and supports in the research group for last few years. I am truly grateful to Dr. David Poyner and Prof. Ian Martin for their inspiring teachings on this subject area in my undergraduate years. My gratitude goes to Rosemary for her conscientious hard work in looking after laboratories, equipments, and students; and to Eva, David, Karthik, Prof.