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Cytosolic glucocorticoid receptors in the developing rat heart
S E Katz1, Z J Penefsky, M Y McGinnis
1Department of Anatomy, Mount Sinai School of Medicine, CUNY 10029.
Journal of Molecular and Cellular Cardiology
|April 1, 1988
Summary
Neonatal glucocorticoid exposure alters rat heart function, suggesting receptor involvement. However, direct receptor binding in neonatal rat hearts was not affected by this early-life treatment.
Area of Science:
- Cardiology
- Endocrinology
- Developmental Biology
Background:
- Glucocorticoid hormones significantly impact cardiac function.
- Neonatal glucocorticoid treatment in rats alters heart function for weeks, implying neonatal cardiac glucocorticoid receptors (GRs) are involved.
- However, the presence of GRs in neonatal rat hearts has not been previously confirmed.
Purpose of the Study:
- To identify and characterize glucocorticoid receptors in neonatal rat heart cytosol.
- To investigate the effect of early-life hydrocortisone acetate administration on GR binding in the neonatal rat heart.
Main Methods:
- Glucocorticoid receptor binding assays were performed on neonatal rat heart cytosol using [3H] dexamethasone.
- Competition assays and Scatchard analysis were employed to characterize receptor binding.
- Rats received a single hydrocortisone acetate injection on post-natal day 2, with GR binding assessed in 12–14-day-old hearts.
Main Results:
- Saturable, specific, high-affinity glucocorticoid receptor binding was detected in neonatal rat heart cytosol.
- Despite altered cardiac function in treated 12–14-day-old rats, hydrocortisone acetate injection on post-natal day 2 did not alter cytosol GR binding in these hearts.
Conclusions:
- Glucocorticoid receptors are present in the neonatal rat heart cytosol.
- Early-life glucocorticoid exposure may alter cardiac function through mechanisms other than direct modulation of GR binding levels in the neonatal period.
- Permanent organizational effects on cardiac tissue due to neonatal glucocorticoid exposure are postulated.