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Effet De L'Hormone De Croissance Sur L'Excretion Renale Des Phosphates

 

作者: CorvilainJ.,  

 

期刊: Acta Clinica Belgica  (Taylor Available online 1966)
卷期: Volume 21, issue sup3  

页码: 2-106

 

ISSN:1784-3286

 

年代: 1966

 

DOI:10.1080/17843286.1966.11716628

 

出版商: Taylor&Francis

 

数据来源: Taylor

 

摘要:

SummaryBesides its well known effect on nitrogen, potassium, sodium and calcium urinary excretion, growth hormone (G.H.) markedly affects phosphorus metabolism: it decreases phosphate excretion and increases the plasma level of phosphorus.Looking for an explanation of this phenomenon, we have studied the effect of G.H. on renal hemodynamics and tubular reabsorption of phosphate.We have observed that G.H. increased in man, after a four days treatment, the renal plasma flow and the glomerular filtration rate (G.F.R.), the filtration fraction remaining constant. We have also confirmed that bovine G.H. increased glomerular filtration rate in the dog.The effect on hemodynamics seems to be linked to sodium retention, for it is not observed in dogs put on a low salt intake.G.H. increased tubular maximal reabsorption of phosphate (TmPO4and the ratio TmPO4/G.F.R., in man and dog.Statistical analysis of our results shows that there is a relationship between Tn.PO, and G.F.R. when G.F.R. varies spontaneously.The same relationship was observed when G.F.R. increased under G.H. influence. However, the increase in G.F.R. was not sufficient to account for the rise in TmPO4observed after G.H. treatment. Moreover, when the rise in G.F.R. was completely prevented by previous administration lo the experimental dogs of a low salt diet, a direct action of G.H. on phosphate reabsorption became clearly apparent.The effect of G.H. on tubular transport of phosphate is not due to the inhibition of parathyroids, since it is not prevented by surgical removal of those glands. This effect is not secondary to a diminution of the action of parathyroid hormone on tubular cells, for previous administration of G.H. does not decrease the efficiency of parathyroid extracts. It is not likely explained either by hypertrophy of the proximal tubules, since G.H. does not increase tubular rcabsorption of glucose in the same proportion.The action of G.H. on tubular reabsorption of phosphate is responsible for the phosphate retention and the increase in plasma phosphorus observed during our metabolic studies. Neither of these phenomenon appeared after G.H. administration in a case of Fanconi syndrome in which histological alterations of the proximal tubuli were demonslrated by renal biopsy.The same modification of the renal capacity for phosphate reabsorption is seen in active acromegaly and in children before puberty. In these two groups. TmPO4per surface unit, the ratio TmP04/G.F.R. and the plasma level of phosphorus are higher than in normal adults. These particularities may be explained, at least in part, by a greater secretion of G.H.

 

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