TY - JOUR
T1 - Mechanisms of endothelin-1-induced contraction in isolated placental veins from normal full-term and preterm pregnancies
AU - Gallardo, Victoria
AU - Antonieta Cruz, M.
AU - Miguel, Patricia
AU - Carrasco, Gonzalo
AU - González, Clemente
N1 - Funding Information:
This research was supported by grants no. 1980132 and 2970098, Fondo Nacional de Ciencia y Tecnologı́a, FONDECYT, Chile. We are very grateful for the assistance provided to us by the personnel of the Labor and Delivery Unit and the physicians of the Service of Obstetrics and Gynecology at G. Grant Benavente Hospital, Concepción, Chile.
PY - 2000
Y1 - 2000
N2 - This study characterizes the reactivity of human chorionic plate vein in full-term (39.4±0.3 weeks of gestation) and preterm (34.4±0.6 weeks of gestation) pregnancy to endothelin-1 (ET-1) and attempts to characterize ET-1 receptor subtype, and the contribution of nitric oxide and cyclooxygenase products in these responses. In placental veins from full-term and preterm pregnant women, cumulative addition of ET-1 (10 -10-10 -6 M) caused marked and long-lasting concentration-dependent contractile responses. The mean EC 50 and E max values for ET-1-induced venoconstriction did not differ between the full-term and preterm pregnancy groups. In the veins from preterm placental preparations, the ET A receptor-selective antagonist cyclo(D-α-aspartyl-L-propyl-D-valyl-L-leucyl-D-tryptophyl (BQ123) reduced the ET-1-induced contraction by 28.6±2.4%, compared to a decline in tension of 51.2±4.2% in the full-term placental vessels. The ET B receptor-selective antagonist, N-[N-[N-[2,6-dimethyl-1piperidinyl)carbonyl]-4-methyl-L-leucyl]-1- (methoxycarbonyl)-D-tryptophyl]-D-norleucinemonosodium (BQ788), did not influence ET-1-induced contraction in placental vein from both pregnancy groups in terms of maximal contraction and sensitivity. Pretreatment with the cyclooxygenase inhibitor, indomethacin (1 μM) and the nitric oxide synthase inhibitor N w-nitro-L-arginine (NOLA, 100 μM) did not significantly affect either the EC 50 or the maximum contraction to ET-1 in veins from normal full-term and preterm preparations. The results of this study suggest that there is no correlation between ET-1-induced vasoconstriction and gestational age and that this vasoconstriction is mediated predominantly via ET A receptor subtype in both groups of pregnant women, independent of NO and eicosanoids.
AB - This study characterizes the reactivity of human chorionic plate vein in full-term (39.4±0.3 weeks of gestation) and preterm (34.4±0.6 weeks of gestation) pregnancy to endothelin-1 (ET-1) and attempts to characterize ET-1 receptor subtype, and the contribution of nitric oxide and cyclooxygenase products in these responses. In placental veins from full-term and preterm pregnant women, cumulative addition of ET-1 (10 -10-10 -6 M) caused marked and long-lasting concentration-dependent contractile responses. The mean EC 50 and E max values for ET-1-induced venoconstriction did not differ between the full-term and preterm pregnancy groups. In the veins from preterm placental preparations, the ET A receptor-selective antagonist cyclo(D-α-aspartyl-L-propyl-D-valyl-L-leucyl-D-tryptophyl (BQ123) reduced the ET-1-induced contraction by 28.6±2.4%, compared to a decline in tension of 51.2±4.2% in the full-term placental vessels. The ET B receptor-selective antagonist, N-[N-[N-[2,6-dimethyl-1piperidinyl)carbonyl]-4-methyl-L-leucyl]-1- (methoxycarbonyl)-D-tryptophyl]-D-norleucinemonosodium (BQ788), did not influence ET-1-induced contraction in placental vein from both pregnancy groups in terms of maximal contraction and sensitivity. Pretreatment with the cyclooxygenase inhibitor, indomethacin (1 μM) and the nitric oxide synthase inhibitor N w-nitro-L-arginine (NOLA, 100 μM) did not significantly affect either the EC 50 or the maximum contraction to ET-1 in veins from normal full-term and preterm preparations. The results of this study suggest that there is no correlation between ET-1-induced vasoconstriction and gestational age and that this vasoconstriction is mediated predominantly via ET A receptor subtype in both groups of pregnant women, independent of NO and eicosanoids.
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U2 - 10.1016/S0306-3623(00)00070-7
DO - 10.1016/S0306-3623(00)00070-7
M3 - Article
C2 - 11368884
AN - SCOPUS:0034443221
SN - 0306-3623
VL - 34
SP - 295
EP - 301
JO - General Pharmacology: The Vascular System
JF - General Pharmacology: The Vascular System
IS - 5
ER -