title: The evolutionary origin of the vasopressin/V2-type receptor/aquaporin axis and the urine-concentrating mechanism.
abstract: In this mini-review, current evidence for how the vasopressin/V2-type receptor/aquaporin axis developed co-evolutionary as a crucial part of the urine-concentrating mechanism will be presented. The present-day human kidney, allowing the concentration of urine up to a maximal osmolality around 1200 mosmol kg(-1)-or urine to plasma osmolality ratio around 4-with essentially no sodium secreted is the result of up to 3 billion years evolution. Moving from aquatic to terrestrial habitats required profound changes in kidney morphology, most notable the loops of Henle modifying the kidneys from basically a water excretory system to a water conserving system. Vasopressin-like molecules has during the evolution played a significant role in body fluid homeostasis, more specifically, the osmolality of body liquids by controlling the elimination/reabsorption of fluid trough stimulating V2-type receptors to mobilize aquaporin water channels in the renal collector tubules. Recent evidence supports that all components of the vasopressin/V2-type receptor/aquaporin axis can be traced back to early precursors in evolutionary history. The potential clinical and pharmacological implications of a better phylogenetic understanding of these biological systems so essential for body fluid homeostasis relates to any pathological aspects of the urine-concentrating mechanism, in particular deficiencies of any part of the vasopressin-V2R-AQP2 axis causing central or nephrogenic diabetes insipidus-and for broader patient populations also in preventing and treating disturbances in human circadian regulation of urine volume and osmolality that may lead to enuresis and nocturia.
authors.affiliation: Clinical R&D, Medical Science Urology, Ferring International Pharmascience Center, 11 Kay Fiskers Plads, 2300, Copenhagen S, Denmark. kvj@ferring.com
authors.forename: Kristian Vinter
authors.initials: KV
authors.lastname: Juul
mesh_terms: D000818:Animals; D051399:Aquaporin 2 / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D020346:Aquaporins / Q000235:genetics* / Q000378:metabolism / Q000502:physiology; D019143:Evolution, Molecular; D006801:Humans; D007671:Kidney Concentrating Ability / Q000235:genetics*; D008954:Models, Biological; D017483:Receptors, Vasopressin / Q000235:genetics* / Q000378:metabolism / Q000502:physiology; D015398:Signal Transduction / Q000235:genetics; D014556:Urine / Q000737:chemistry / Q000502:physiology
chemical_list: D051399:Aquaporin 2; D020346:Aquaporins; D017483:Receptors, Vasopressin