Changes of urine formation function caused by ammonium molybdate in intact rats and in experimental hypercalcemia

AIM: to study of influence of ammonium molybdate on urine formation function of kidneys in modeling of the experimental hypercalcaemia on white rats. MATERIAL AND METHODS. Ammonium molybdate (50 mg/kg) was introduced through a probe into a stomach of the intact rats daily within a month. Hypercalcaemia was created by intragastric introduction of 10% calcium chloride solution (0,15 ml on 100 g of body weight) within a month. Studying of the main processes of a urine formation, indicators of a cortex-papillary gradient of urea and sodium concentration in layers of renal tissues, the analysis of the blood content of electrolytes (sodium, potassium, calcium) and their kidney processing was carried out in the conditions of 6 hour spontaneous diuresis and 3-hour water diuresis. RESULTS. Introduction of ammonium molybdate leads to the violation of ion-water excretory renal function, causing poliuria, proteinuria, decrease in a tubular reabsorption of sodium and calcium, increasing their excretion and promoting hyponatremiya development; has kaliuretic and hyperkaliemic effect. Reduction of urine osmolarity in conditions of the renal cortex-papillary osmotic gradient reduction and decrease in tubular transport of osmotically free water Т^CН₂O in the conditions of a poliuria testifies to the violation of renal concentrating function. Molybdenum introduction in the conditions of hyperhydratation reduced the percent of the removal of water loading, owing to increase in a tubular reabsorption of water with less effective decrease in a cortex-papillary osmotic gradient. Functional ability of kidneys to the removal of excess liquid from the organism and to osmotic dilution decreased in molybdenic intoxication. Use of calcium chloride promoted reduction of the expressiveness of ion-osmoregulatory renal function indicators changes, restoring level of the excretion of electrolytes, osmotic purification of plasma and an excretion of osmotically free water. CONCLUSION. The experimental model of a hypercalcaemia softens the expressiveness of nephrotoxic effects of molybdenum, has beneficial impact on the safety of the renal functional state and concentrating ability indicators that can testify to the mutually competitive relations between calcium and molybdenum.

molybdenum, hypercalcaemia, poliuria, proteinuria

1. Реутова Н.В. Анализ заболеваемости населения в районе расположения вольфрамомолибденового комбината. Гиг. и санит. 2007; 4: 13-15

2. Pandey, R. Kumar. Molybdenum toxicity. Human & Experimental Toxicology 2009: 33-35.

3. Бельмер С.В., Гасилина Т.В. Микроэлементы и микроэлементозы и их значение в детском возрасте. Вопр современной педиатрии 2008; 7(6) 91-96.

4. Ohta H., Yamauchi Y., Nakakita M., Tanaka H. Relationship between renal dysfunction and bole metabolism disorder in male rats after long-term oral quantitative cadmium administration. Ind Health 2000; 38(4): 339-355.

5. Скальный А.В. Химические элементы в физиологии и экологии человека. М.: Издательский дом «ОНИКС 21 век»: Мир, 2004; 25-31; 123.

6. Цаллаева Р.Т., Брин В.Б. Эффекты хлорида цинка на функцию почек у паратиреидэктомированных крыс. Вестник новых медицинских технологий 2013; 20 (2): 375-377.

7. Брин В.Б., Ахполова В.О., Хадарцева М.П. и др. Почечные эффекты тяжелых металлов в условиях измененного обмена кальция. XXI съезд Физиологического общества им. И.П. Павлова. Тез. докл. (Волгоград. 16-20 сентября 2013). Москва-Волгоград, 2013.

8. Албегова Ж.К., Брин В.Б., Гаглоева Э.М., Закс Т.В. Почечные проявления хронической молибденовой интоксикации. Вест международной академии наук экологии и безопасности жизнедеятельности 2010; 15; (4); 85-88.

9. Наточин Ю.В. Физиология почки: формулы и расчеты. Наука. Л., 1974; 56.

10. Боголепова А.Е., Наточин Ю.В. Физиологический анализ функций почки при различных типах диуреза. Нефрология 2005; 9 (2); 9-15.