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Decrease in the response to ADH of the rat kidney as a result of early postnatal treatment with cortisol
Pflugers Archiv : European Journal of Physiology
|April 1, 1987
Summary
Early life cortisol exposure in Wistar rats impairs the development of antidiuretic hormone (ADH) response, affecting kidney function and cAMP signaling pathways. This disruption persists into adulthood, highlighting long-term consequences of neonatal stress.
Area of Science:
- Endocrinology
- Developmental Biology
- Nephrology
Background:
- Neonatal exposure to glucocorticoids can impact organ development and function.
- Antidiuretic hormone (ADH) plays a crucial role in regulating water balance in the kidneys.
Purpose of the Study:
- To investigate the long-term effects of a single neonatal cortisol injection on the development of ADH response in Wistar rats.
- To explore the underlying mechanisms involving AVP binding and cAMP signaling.
Main Methods:
- Wistar rats received a single intraperitoneal injection of cortisol or saline on day 5 of life.
- Urine/plasma osmolality (U/P)osm ratio and response to ADH were assessed at various ages.
- Specific binding of (3H)AVP and cAMP in kidney tubule fragments and cytosolic fractions were measured.
Main Results:
- Cortisol-treated rats showed a weaker and delayed response to ADH compared to controls, persisting up to 60 days of life.
- Reduced (3H)AVP specific binding was observed in collecting tubules of cortisol-treated rats at 20 and 60 days.
- Altered ontogenetic patterns of cAMP specific binding and decreased cytosolic protein kinase activity were noted in cortisol-exposed rats.
Conclusions:
- Neonatal cortisol exposure interferes with the ontogenetic development of AVP binding capacity and cAMP-dependent protein kinase.
- This interference is a plausible cause for the altered development of the ADH response in rats.
- The findings suggest critical windows during development where hormonal exposure can have lasting effects on kidney function.