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Sex differences in prenatal programming of hypertension by dexamethasone
Issa Alhamoud1, Susan K Legan1, Jyothsna Gattineni1
1Department of Pediatrics, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-9063, USA.
Prenatal dexamethasone exposure elevates blood pressure and causes kidney damage in male offspring, but not females. This hypertension is not linked to changes in renal transporters or the renin-aldosterone system.
Area of Science:
- Endocrinology
- Developmental Biology
- Nephrology
Background:
- Prenatal exposure to synthetic glucocorticoids like dexamethasone can impact offspring development.
- Previous studies indicate dexamethasone increases blood pressure in male offspring, but the underlying mechanisms remain unclear.
Purpose of the Study:
- To investigate if prenatal dexamethasone exposure affects blood pressure similarly in male and female offspring.
- To determine if hypertension in offspring is associated with changes in renal tubular transporters or the renin-aldosterone system.
Main Methods:
- Pregnant rats received dexamethasone on specific gestational days.
- Offspring blood pressure, proteinuria, and albuminuria were assessed at different ages.
- Renal tubular transporter protein abundance, plasma renin, and serum aldosterone levels were measured.
Main Results:
- Prenatal dexamethasone increased blood pressure and induced proteinuria/albuminuria in male offspring at two and six months, but not in females.
- A transient increase in the sodium-potassium-two-chloride cotransporter was observed in males at two months.
- No significant alterations in other renal transporters, renin, or aldosterone were found.
Conclusions:
- Prenatal dexamethasone exposure leads to hypertension and kidney dysfunction specifically in male offspring.
- The observed hypertension is not consistently mediated by alterations in renal tubular transporters or the renin-aldosterone system.
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