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Attenuation of the vasoconstrictor effects of thromboxane and endothelin by nitric oxide in the human fetal-placental circulation
Ist Teil von
American journal of obstetrics and gynecology, 1992, Vol.166 (1), p.224-230
Ort / Verlag
Philadelphia, PA: Mosby, Inc
Erscheinungsjahr
1992
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
Objective: We hypothesized that the endothelial-derived relaxing factor nitric oxide may contribute to low resting vascular tone and may attenuate vasoconstrictor action in the human fetal-placental circulation.
Study design: Isolated human placental cotyledons were dually perfused in vitro, and the effects of N-monomethyl-
L-arginine and N-nitro-
L-arginine (3 × 10
−4 mol/L), which are nonmetabolizable analogs of L-arginine, the substrate for nitric oxide synthase, on resting perfusion pressure and on the fetal-placental circulation preconstricted with U46619 (10
−8 mol/L) or endothelin-1 (10
−8 mol/L) were established. Responses before and after inhibition were compared by paired f test. The effects of glyceryl trinitrate (10
−6 mol/L), acetylcholine (10
−4 mol/L), the calcium ionophore A23187 (10
−6 mol/L), and histamine (10
−8 to 10
−4 mol/L) were also determined in the preconstricted fetal-placental circulation.
Results: Both N-monomethyl-
L-arginine and N-nitro-
L-arginine (3 × 10
−4 mol/L) increased resting perfusion pressure (
p < 0.06), and N-nitro-
L-arginine promptly and significantly increased perfusion pressure in the fetal-placental circulation preconstricted with U46619 (
p < 0.0004) or endothelin-1 (
p < 0.06). Nitric oxide generated by addition of glyceryl trinitrate (10-6 mol/L) attenuated the vasoconstrictor effects of U46619 (
p < 0.026) or endothelin-1 (
p < 0.01). Neither acetylcholine nor the calcium ionophore A23187 had an effect on the fetal-placental circulation, whereas bradykinin further increased perfusion pressure. Histamine only relaxed the preconstricted preparations at concentrations (10
−6 to 10
−4 mol/L) above those shown to release nitric oxide in other systems.
Conclusion: The stimulus to nitric oxide generation in the fetal-placental circulation may be hydrodynamic. Nitric oxide appears to contribute to maintenance of basal vascular tone and to attenuate the actions of vasoconstrictors in this circulation.