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Research Article Free access | 10.1172/JCI108274

A renotropic system in rats.

H G Preuss and H Goldin

Find articles by Preuss, H. in: PubMed | Google Scholar

Find articles by Goldin, H. in: PubMed | Google Scholar

Published January 1, 1976 - More info

Published in Volume 57, Issue 1 on January 1, 1976
J Clin Invest. 1976;57(1):94–101. https://doi.org/10.1172/JCI108274.
© 1976 The American Society for Clinical Investigation
Published January 1, 1976 - Version history
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Abstract

While plasma or sera obtained from rats 20 h after removal of one kidney (uninephrectomy) stimulated [3H] thyrmidine incorporation into the DNA of kidney tissue incubating in vitro, azotemic plasma or sera obtained from rats 20 h after removal of both kidneys had no apparent effect. Dialysis of this azotemic sera resulted in its ability to stimulate isotope incorporation into renal DNA to the same degree as sera from uninephrectomized rats. This stimulatory factor (renotropin) was found to rise significantly within the first 26 h after uninephrectomy. Renotropin worked only on renal tissue, and we found that a factor could be extracted in large amounts from the remaining kidney 20 h after uninephrectomy that would stimulate renal DNA synthesis in the presence of sera. Based on these findings and others, we postulate that after uninephrectomy there is an elevation in circulating renotropin as well as a tissue factor in the remaining kidney. Both factors together probably produce an excitor which enhances [3H] thymidine into DNA. The latter is tightly bound to renal tissue, and its production and/or activity is modified by circulating inhibitors that are especially prominent in azotemia.

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