Abstract
Renal compensatory hypertrophy (RCH) occurs in hypothyroid rats, 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 hyper-adrenocorticism: it is related to an increased plasma testosterone level and to a disturbed Na +, K + and glucose metabolism.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
