ANTENATAL BETAMETHASONE THERAPY POTENTIATES NITRIC OXIDE-MEDIATED RELAXATION OF PRETERM OVINE CORONARY-ARTERIES

The present study was designed to test the hypothesis that betamethaso ne may potentiate nitric oxide-mediated relaxation of coronary arterie s of preterm lambs. Isolated coronary arteries were obtained from lamb s delivered at 128 days gestation. The lambs were treated intramuscula rly with a single dose of betamethasone or saline 48 h before delivery and were killed after 3 h of ventilation after delivery. Vessel rings were suspended in organ chambers filled with modified Krebs-Ringer so lution (95% O-2-5% CO2, 37 degrees C), and their isometric tension was recorded. The endothelium-dependent relaxation induced by bradykinin and calcium ionophore A23187 was greater in arteries from antenatal be tamethasone-treated lambs than in arteries from control lambs. The rel axation was abolished by N-w-nitro-L-arginine. Nitric oxide induced a greater relaxation in vessels from antenatal betamethasone-treated lam bs and in vessels preincubated with betamethasone than in vessels from controls. Coronary arteries from control and antenatal betamethasone- treated lambs relaxed similarly to 8-bromoguanosine 3',5'-cyclic monop hosphate. Nitric oxide induced a greater increase in guanosine 3',5'-c yclic monophosphate content in coronary arteries from antenatal betame thasone-treated lambs than in arteries from control lambs. Our data su ggest that antenatal betamethasone therapy potentiates nitric oxide-me diated relaxation in coronary arteries from preterm lambs, probably by affecting the activity of soluble guanylate cyclase of vascular smoot h muscle cells.