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Hyperactive Vasopressin Receptors and Disturbed Water Homeostasis Nine V.A.M

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Hyperactive Vasopressin Receptors and Disturbed Water Homeostasis Nine V.A.M PERSPECTIVE The Calling school, coming to the profession for timeless rea- rate life events from their meaning for those who sons — because of a physician they admire, or be- live them. In literature, the two are united. That is cause they want to serve, or because they have suf- reason enough to keep reading. And writing. fered or witnessed suffering. Perhaps some lucky ones even today have been called to medicine 1. Maugham WS. Of human bondage. New York: Bantam Books, 1991. through the medium of a book. If they have a love 2. Fraser A, ed. The pleasure of reading. London: Bloomsbury, of literature, reading may well help them to discov- 1992:74-8. er a way to understand and identify with the ambi- 3. Trautmann J. The wonders of literature in medical education. Mobius 1982;2(3):23-31. tions, sorrows, and joys of the people whose lives 4. Allison D. Skin: talking about sex, class & literature. Ithaca, are put in their hands. In medicine, we often sepa- N.Y.: Firebrand Books, 1994. Hyperactive Vasopressin Receptors and Disturbed Water Homeostasis Nine V.A.M. Knoers, M.D., Ph.D. Related article, page 1884 Regulation of water homeostasis is of vital impor- diated activation of adenylate cylase and the forma- tance for all terrestrial organisms. In most mam- tion of cyclic adenosine monophosphate (cAMP). mals, including humans, the maintenance of water cAMP, in turn, activates protein kinase A, which pro- balance is critically dependent on water intake, the motes the fusion of cytoplasmic vesicles containing sensation of thirst, and the regulation of water ex- aquaporin-2 water-channel proteins with the apical cretion in the kidney, which is under the control membrane. As a result, this normally water-tight of the antidiuretic hormone arginine vasopressin membrane becomes water-permeable. Driven by (AVP).1 In the past decade, our insight into the the osmotic gradient of sodium, water is then trans- AVP-mediated renal concentration mechanism has cellularly reabsorbed, entering the cells through substantially improved with the elucidation of the aquaporin-2 in the apical membrane and leaving roles of crucial molecular players in this process. the cells for the interstitium through aquaporin-3 The identification of disease-causing genes in he- and aquaporin-4, which reside in the basolateral reditary disorders of water balance has been ex- membrane. The withdrawal of AVP results in en- tremely helpful in identifying these pivotal mole- docytosis of the water channels, restoring the wa- cules. ter-impermeable state of the apical membrane. In normal physiology, AVP is secreted into the Proof of principle for the critical roles of both circulation by the posterior pituitary gland, in re- the V2 receptor and aquaporin-2 in orchestrating sponse to an increase in serum osmolality or a de- the AVP-mediated renal concentration mechanism crease in effective circulating volume (see diagram). came from the identification of mutations in the In the kidney, AVP binds to the V2 vasopressin genes encoding these proteins in patients with reeptor in the basolateral membranes of collect- congenital nephrogenic diabetes insipidus.2 This ing-duct cells in the last portion of the nephron rare genetic disorder is characterized by a failure to (see diagram). Occupancy of this receptor results, concentrate urine despite normal or elevated levels by means of signaling through a guanine nucleo- of AVP. Polyuria and polydipsia, usually associated tide–binding regulatory protein (G protein), in me- with hypernatremia, are typical features of this dis- order. The disease is particularly serious in infants, Dr. Knoers is a professor of clinical genetics at the Depart- in whom recurrent episodes of dehydration may re- ment of Human Genetics, Radboud University Nijmegen sult in severe neurologic deficits, growth retarda- Medical Centre, Nijmegen, the Netherlands. tion, or even death. Mutations in the gene encod- n engl j med 352;18 www.nejm.org may 5, 2005 1847 The New England Journal of Medicine Downloaded from www.nejm.org at CTR HOSPITAL UNIVERSITAIRE VAUDOIS on November 6, 2010. For personal use only. No other uses without permission. Copyright © 2005 Massachusetts Medical Society. All rights reserved. PERSPECTIVE Hyperactive Vasopressin Receptors and Disturbed Water Homeostasis A Increased plasma osmolality or decreased arterial circulating volume Thirst Increased fluid intake Decreased plasma osmolality or increased arterial circulating volume AVP Antidiuresis SIADH B Collecting Autosomal recessive and tubule dominant CNDI H2O H2O Aquaporin-4 Aquaporin-3 H2O H O H O channel H O channel 2 2 2 Aquaporin-2 H2O channel Stimulating G protein cAMP Vasopressin Protein type 2 receptor kinase A Arginine ATP vasopressin Adenylate cyclase Phosphoproteins Inactivating mutations: X-linked CNDI Activating mutations: NSIAD H2O H2O H2O Basolateral Apical Physiology of Water Homeostasis in Humans (Panel A) and Pathway of AVP Signaling in Renal Collecting-Duct Cells Involved in Regulating Water Excretion (Panel B). The cells of the collecting duct are polarized into an apical surface that faces the lumen of the collecting duct, through which the tubular fluid flows, and a basolateral surface that faces the circulating blood. The relevant disorders of water balance include the syndrome of inappropri- ate antidiuretic hormone secretion (SIADH), congenital nephrogenic diabetes insipidus (CNDI), and nephrogenic syndrome of inappropriate antidiuresis (NSIAD). The aquaporin-2 water channel is regulated by vasopressin, and the aquaporin-3 and aquaporin-4 water channels are constitutively expressed. AVP denotes arginine vasopressin, and cAMP cyclic adenosine monophosphate. 1848 n engl j med 352;18 www.nejm.org may 5, 2005 The New England Journal of Medicine Downloaded from www.nejm.org at CTR HOSPITAL UNIVERSITAIRE VAUDOIS on November 6, 2010. For personal use only. No other uses without permission. Copyright © 2005 Massachusetts Medical Society. All rights reserved. PERSPECTIVE Hyperactive Vasopressin Receptors and Disturbed Water Homeostasis matic mutations that have been identified in certain Diseases Caused by Activating (Gain-of-Function) Mutations adenomas and malignant tumors. Such activating in G Protein–Coupled Receptors. mutations with germ-line transmission have been Disease G Protein–Coupled Receptor identified in only a few inherited disorders (see table). Testotoxicosis (familial male-limited pre- Luteinizing hormone receptor cocious puberty) (LHR) At present, more than 180 different mutations in AVPR2 have been described. These mutations all Autosomal dominant nonimmune hyper- Thyrotropin receptor (TSHR) thyroidism cause congenital nephrogenic diabetes insipidus and, consistently, are inactivating mutations, re- Congenital stationary blindness Rhodopsin sulting in receptor malfunction at different lev- Autosomal dominant hypocalcemia Calcium-sensing receptor (CaSR) els, such as reduced receptor expression at the cell Corticotropin-independent Cushing’s Melanocortin-2 receptor (MC2R) surface or disturbances in hormone binding and syndrome G protein coupling. Familial ovarian hyperstimulation Follitropin receptor (FSHR) In this issue of the Journal (pages 1884-1890), syndrome Feldman and coauthors describe two unrelated Jansen’s metaphyseal chondrodysplasia Parathyroid hormone/parathy- male infants with euvolemic hyponatremia and se- roid hormone–related pro- tein (PTH/PTHrP) receptor rum hypo-osmolality, along with inappropriately elevated urine osmolality and urine sodium con- Nephrogenic syndrome of inappropriate Vasopressin type 2 receptor antidiuresis (NSIAD) (V2R) centrations. At first glance, the disorder in these boys resembles the syndrome of inappropriate an- tidiuretic hormone secretion (SIADH), a relatively common disorder characterized by insufficient ing the V2 receptor (AVPR2) cause the X-linked form suppression of AVP secretion in relation to the de- of congenital nephrogenic diabetes insipidus, and gree of hypo-osmolality, which leads to inappropri- mutations in the gene encoding aquaporin-2 are ate urine concentration. Since serum AVP levels responsible for both the autosomal recessive and were undetectably low in both boys, Feldman et al. autosomal dominant forms. ruled out SIADH and hypothesized that a hyperac- The V2 receptor is a typical member of the large tive V2 receptor could be the underlying cause of superfamily of G protein–coupled receptors, which the disorder. Sequencing of AVPR2 in the two pa- includes receptors for hormones, neurotransmit- tients revealed a hemizygous point mutation in ters, light, odorants, lipids, and ions. Once an ago- each. In an in vitro functional assay, both muta- nist binds to such a receptor, an intracellular signal tions were shown to lead to the production of a cascade is induced through the coupling and acti- constitutively active V2 receptor. The consequence vation of a G protein. G protein–coupled receptors was AVP-independent, and therefore inappropri- play key roles in almost all physiological functions, ate, activation of V2 receptor–mediated renal urine and mutations in the genes encoding these recep- concentration. Remarkably, and for reasons that tors have been identified in patients with a variety remain unexplained, neither patient showed any of inherited and acquired disorders, such as retini- clinical or biochemical sign of constitutive activa- tis pigmentosa, hypothyroidism and hyperthyroid- tion of extrarenal V2 receptors, which are known to ism, dwarfism, fertility disorders, obesity, and
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