[Pathogenesis of lithium polyuria].
An attempt is made to elucidate the pathogenesis of polyuria arising consequent upon medication of affective states with lithium salts. Experiments conducted with 54 male-rats showed that changes in the neurosecretion of supraoptic nuclei of the hypothalamus and neurohypophysis that take place after a course-wise intraperitoneal administration in amounts of 200 mg/kg (2/9DL20) of lithium chloride per 24 hours for a duration of 6 days occur parallel with histochemical changes of renal acid muconpolysaccharides and they accord with the nature of diuresis disorders. By the 5th day of the experiment the compound perverts the antidiuretic effect of a single subcutaneous injection of pituitrin (10 U/kg). The authors infer therefrom that polyuria emerging after introduction of lithium salts is caused by a deranged synthesis and secretion of the diuretic hormone and also by the ability of lithium to mitigate the action of this hormone on the kidneys.
D000818:Animals; D006025:Glycosaminoglycans / Q000378:metabolism; D006651:Histocytochemistry; D007668:Kidney / Q000378:metabolism; D008094:Lithium / Q000633:toxicity*; D008297:Male; D009489:Neurosecretion; D010904:Pituitary Gland, Posterior / Q000378:metabolism; D011141:Polyuria / Q000139:chemically induced*; D012313:RNA / Q000378:metabolism; D051381:Rats; D013495:Supraoptic Nucleus / Q000378:metabolism; D014667:Vasopressins / Q000378:metabolism
D006025:Glycosaminoglycans; D014667:Vasopressins; D012313:RNA; D008094:Lithium
O pathogeneze litievoĭ poliurii