Effect of vanadate on renal tubular function in rats
Autor: | R. K. Hamburger, Christof Westenfelder, M. E. Garcia |
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Rok vydání: | 1981 |
Předmět: |
Male
medicine.medical_specialty Physiology Blood Pressure Nephron Urine Renal chloride reabsorption Natriuresis Phosphates Body Water Internal medicine medicine Cyclic AMP Animals Reabsorption Chemistry Vanadium Effective renal plasma flow Renal glucose reabsorption Rats Free water clearance Bicarbonates medicine.anatomical_structure Endocrinology Glucose Kidney Tubules Renal physiology Vanadates Diabetes Insipidus Glomerular Filtration Rate |
Zdroj: | The American journal of physiology. 240(6) |
ISSN: | 0002-9513 |
Popis: | Orthovanadate (VO4) has been shown to cause a marked natriuresis in rats. This has been ascribed to its inhibitory action on renal Na-K-ATPase activity. Because virtually all nephron segments possess Na-K-ATPase activity the administration of VO4 should alter renal tubular transport along the entire nephron. To examine this possibility, adult rats were anesthetized and infused with VO4 (10 mumol.kg body wt-1.h-1 i.v.). This dose had no effect on glomerular filtration rate, effective renal plasma flow, and blood pressure, whereas urine flow and sodium and water excretion rose markedly. Potassium excretion remained unaltered. VO4 depressed only maximal bicarbonate and glucose reabsorption without causing a glucose or bicarbonate "leak" at normal levels of blood glucose or bicarbonate. In acutely thyroparathyroidectomized rats VO4 produced a striking phosphaturia, not accompanied by an increase in nephrogenous cAMP excretion. Both free water clearance in Brattleboro rats and free water reabsorption in normal rats was significantly depressed by VO4. These data demonstrate that VO4 depresses tubular reabsorption in proximal and distal nephron segments. We conclude that VO4 exerts its effect on tubular function by inhibition of Na-K-ATPase activity. |
Databáze: | OpenAIRE |
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