Abstract
Low birth weight in combination with a large placenta predicts human hypertension. The pathophysiological link remains unclear, but glucocorticoid excess impairs fetal growth and leads to offspring hypertension. A key controller of fetal glucocorticoid exposure and local tissue availability is 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). The activity of placental 11β-HSD2 correlates with fetal growth in animals and humans. Ethanol abuse and smoking are known to retard fetal growth which may relate to altered glucocorticoid action or dynamics. This study has examined whether nicotine or ethanol modulate glucocorticoid action in the placenta or fetus by inhibiting 11β-HSD2, using clonal cell cultures, freshly isolated dually perfused intact human placentas and placentas from in vivo treated rats. No significant effect on the activity of 11β-HSD2 by pathophysiologically relevant nicotine or ethanol concentrations was observed. The mechanism of action of nicotine and ethanol relevant to reduced fetal growth requires further study.
| Original language | English |
|---|---|
| Pages (from-to) | 303-307 |
| Number of pages | 5 |
| Journal | Journal of Steroid Biochemistry and Molecular Biology |
| Volume | 63 |
| Issue number | 4-6 |
| DOIs | |
| Publication status | Published - Nov 1997 |
Bibliographical note
Funding Information:Acknowledgements--This work has been supported by a Wellcome Trust Advanced Training Fellowship (RB) a Wellcome Senior Clinical Fellowship ORS) and grants from the Wellcome Trust, the Scottish Hospital Endowments Research Trust, the Medical Research Council and the Sir Stanley and Lady Davidson Medical Research Fund. We would like to thank Mrs. Jill C. Smith for technical assistance, staff at the Simpson Memorial Maternity Pavilion in Edinburgh for help with help with collecting placentas and Dr. Caroline Leckie for providing LLC-PK1 cells.