title: [The hyperiricosuria as an indicator of derangement of biologic functions of endoecology and adaptation, biologic reactions of excretion, inflammation and arterial tension].
abstract: During millions years in all animals allantoine (oxidized by uricase uric acid) was catabolite of purines and ascorbic acid was an acceptor of active forms of oxygen. The proximal tubules of nephron reabsorbed the trace amounts of uric acid Then during phylogenesis the primates had a mutation of ascorbic acid gen minus. Later on occurred a second spontaneous mutation and uricase gen minus and uric acid became catabolites of purines. In absence of ascorbic acid synthesis ions of urates became a major capturers of active forms of oxygen and all uric acid as before underwent the reabsorption. Later the carriers were formed which began in epithelium of proximal tubules to secrete all uric acid into urine. At every incident of "littering" of intercellular medium with endogenic flogogens (impairment of biologic function of endoecology) under compensatory development of biologic reaction of inflammation the need in inactivation of active forms of oxygen increases. Hence later on in phylogenesis one more stage was formed--post secretory reabsorption of uric acid In the biologic reaction of inflammation epithelium of proximal tubules initiates retentional hyperiricosuria. The general antioxidant activity of human blood plasma in 60% is presented by urates' ions. The excretion of uric acid includes 4 stages: filtration, full reabsorption, secretion and post secretory reabsorption. In phylogenesis these stages formed in sequence. The mild hyperiricosuria is most frequently considered as a non-specific indicator of activation of biologic reaction of inflammation. The productive hyperiricosuria develops more infrequently under surplus of meat food and cytolysis syndrome (intensification of cell loss in vivo). Under concentration of uric acid more than 400 mkmol/l part of urates circulates in intercellular medium in the form of crystals. The microcrystals of uric acid (biologic "litter") initiate the syndrome of systemic inflammatory response as an endogenic flogogen--initiator of inflammation. The uric acid in the form of ion-capturers of active forms of oxygen is involved into in the formation of syndrome of compensatory anti-inflammatory defense. It may be assumed that simultaneously with post-secretory reabsorption of ions of urates in proximal tubules of nephron occurs intensification of philogenetically late post-secretory reabsorption of ions of sodium and activation of of biologic reaction of hydrodynamic and hydraulic pressure in local pool of intravascular medium i.e. arterial tension. The uric acid simultaneously participates in realization of biologic function of endoecology and adaptation, biologic reactions of excretion, inflammation and arterial tension.
authors: V N
authors: VN
authors: Titov
authors: E V
authors: EV
authors: Oshchepkova
authors: V A
authors: VA
authors: Dmitriev
authors: O V
authors: OV
authors: Gushchina
authors: Iu K
authors: IuK
authors: Shiriaeva
authors: A Ia
authors: AIa
authors: Iashin
mesh_terms: D000818:Animals; D062186:Arterial Pressure; D005919:Glomerular Filtration Rate; D006801:Humans; D033461:Hyperuricemia / Q000097:blood / Q000503:physiopathology / Q000652:urine; D007249:Inflammation / Q000097:blood / Q000503:physiopathology / Q000652:urine; D007687:Kidney Tubules, Proximal / Q000378:metabolism / Q000503:physiopathology; D014527:Uric Acid / Q000097:blood / Q000652:urine
chemical_list: D014527:Uric Acid