Abstract：
:Renal compensatory hypertrophy (RCH) occurs in hypothyroid rate, but it is impaired when compared to RCH found in euthyroid controls. It is due to cellular hypertrophy as the DNA content does not change and the Protein/DNA ratio increases in the compensating kidney. RCH is enhanced by thyroxine (T4) with a rise in the DNA content of the compensating kidney, but the Protein/DNA ratio does not change indicating that hypertrophy is as important as hyperplasia. Corticotrophin (ACTH) given to eu and hypothyroid rats enhances RCH with an increase in the protein content of the compensating kidney without any change in its DNA content. In the hyperthyroid rats, the enhanced RCH is not further increased by ACTH and the rise in the kidney DNA content elicited by T4 is suppressed by ACTH. The Protein/DNA ratio is increased by ACTH in hypo, eu and hyperthyroid rats. The renotrophic action of ACTH is due to hyperadrenocorticism: it is related to an increased plasma testosterone level and to a disturbed Na+, K+ and glucose metabolism.
journal_name
Life Scijournal_title
Life sciencesauthors
Stéphan F,Réville P,de Laharpe F,Köll-Back MHdoi
10.1016/0024-3205(82)90278-8subject
Has Abstractpub_date
1982-02-15 00:00:00pages
623-31issue
7-8eissn
0024-3205issn
1879-0631pii
0024-3205(82)90278-8journal_volume
30pub_type
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