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1 Laboratory for Pregnancy and Newborn Research, Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853; and 2 Clinical Pharmacology Unit, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 2QQ, United Kingdom
At
110-111 days gestation, instrumented fetal sheep were administered
saline or dexamethasone (2.2 µg · kg
1 · h1 iv) for
48 h. Measurement of fetal blood pressure showed a greater increase in dexamethasone-treated (n = 6) compared with
control (n = 5) fetuses (7.3 ± 2.3 vs. 0.6 ± 2.3 mmHg, P < 0.05). Fetuses were delivered by
cesarean section, and the femoral muscle and brain were obtained under
halothane anesthesia. Femoral and middle cerebral arteries (~320-µm
internal diameter) were evaluated using wire myography. Sensitivity to
KCl (2.5-125 mM) and the magnitude of the maximal vasoconstriction
to 125 mM K+ were similar in femoral and middle cerebral
arteries from dexamethasone-treated vs. control fetuses.
Acetylcholine-induced vasorelaxation was similar in femoral arteries
from control and dexamethasone-treated fetuses. Middle cerebral
arteries did not relax to acetylcholine. Sensitivity to endothelin-1
(ET-1; 0.1 pM-0.1 µM) and magnitude of the ET-1-induced
vasoconstriction were greater in femoral arteries from
dexamethasone-treated vs. control fetuses (P < 0.05).
Autoradiographical studies with receptor-specific ligands demonstrated
increased ETA-receptor binding, the principal receptor
subtype, in femoral muscle vessels (P < 0.001) but
decreased ETA-receptor binding in middle cerebral arteries
(P < 0.01) from dexamethasone-treated compared with
control fetuses. Relatively little ETB-receptor binding was
evident in all tissues examined. We conclude that hyperreactivity to
ET-1, due to increased ETA-receptor binding, may be
involved in the dexamethasone-induced increase in peripheral vascular
resistance in fetal sheep in vivo.
glucocorticoids; blood pressure; fetal sheep
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