Prenatal Dexamethasone Programs Autonomic Dysregulation in Female Rats

Area of Science:

• Endocrinology
• Neuroscience
• Cardiovascular Physiology

Background:

• Autonomic dysfunction is linked to cardiovascular and neurological disorders.
• Glucocorticoid exposure during gestation may program autonomic dysfunction.
• Prior studies show dexamethasone exposure increases stress-responsive blood pressure and heart rate in female offspring.

Purpose of the Study:

• To investigate the impact of sympathetic (SYM) or parasympathetic (PS) blockade on cardiovascular function in male and female rat offspring exposed to dexamethasone (DEX) in utero.
• To characterize the autonomic dysregulation induced by prenatal DEX exposure in female offspring.

Main Methods:

• Rat offspring of mothers injected with DEX or vehicle in utero were studied at 11-12 weeks of age.
• Cardiovascular function (MAP, HR, HRV) was assessed at baseline and during SYM or PS blockade.
• Stress-responsive function was evaluated following acute restraint stress.

Main Results:

• Maternal DEX injection reduced basal heart rate variability (HRV) in both male and female offspring.
• Sympathetic blockade attenuated stress-responsive increases in heart rate (HR) and mean arterial pressure (MAP).
• Parasympathetic blockade exacerbated stress-responsive HR and MAP in female offspring, suggesting a shift toward sympathetic dominance.

Conclusions:

• Maternal DEX exposure disrupts autonomic regulation of cardiovascular function in female offspring.
• This disruption results in a shift toward greater sympathetic input and reduced parasympathetic input.
• Prenatal dexamethasone exposure alters the sympathovagal balance in female offspring, impacting cardiovascular responses to stress.