Holcberg G, Kossenjans W, Brewer A, Miodovnik M, Myatt L
Department of Obstetrics and Gynecology, University of Cincinnati College of Medicine, OH 45267-0526.
Am J Obstet Gynecol. 1995 Jan;172(1 Pt 1):71-7. doi: 10.1016/0002-9378(95)90086-1.
Our purpose was to compare the actions of atrial natriuretic peptide and brain natriuretic peptide in the human placental vasculature.
Isolated placental cotyledons were dually perfused with fetal perfusion pressure used as an index of vascular response. The effect of angiotensin II (10(-10) to 10(-6) mol/L bolus injection) was established in the absence or presence of atrial natriuretic peptide (10(-8) mol/L) or brain natriuretic peptide (10(-8) mol/L final concentration). The role of nitric oxide as a mediator of natriuretic peptide action was investigated by perfusion of n-nitro-L-arginine (10(-3) mol/L), an inhibitor of nitric oxide synthase. Attenuation of the action of atrial natriuretic peptide by placental peptidases was studied by perfusion with the peptidase inhibitor benzamidine (2 x 10(-2) mol/L). Statistical significance was determined by analysis of variance and paired t test.
Significant attenuation of vasoconstrictor responses to angiotensin II occurred within both atrial natriuretic peptide and brain natriuretic peptide; however, brain natriuretic peptide was more effective. n-Nitro-L-arginine did not affect the attenuation of angiotensin II-induced vasoconstriction by atrial or brain natriuretic peptides. In the presence of benzamidine atrial natriuretic peptide exerted a significantly greater vasodilator effect.
Brain natriuretic peptide is a more potent vasodilator of the placental vasculature than is atrial natriuretic peptide. The low efficacy of atrial natriuretic peptide may be related to placental peptidases. Nitric oxide does not mediate the action of atrial natriuretic peptide or brain natriuretic peptide.
我们的目的是比较心房利钠肽和脑利钠肽在人胎盘血管系统中的作用。
将分离的胎盘小叶进行双重灌注，以胎儿灌注压作为血管反应指标。在不存在或存在心房利钠肽（10⁻⁸mol/L）或脑利钠肽（终浓度10⁻⁸mol/L）的情况下，确定血管紧张素II（10⁻¹⁰至10⁻⁶mol/L推注）的作用。通过灌注一氧化氮合酶抑制剂n-硝基-L-精氨酸（10⁻³mol/L）来研究一氧化氮作为利钠肽作用介质的作用。通过灌注肽酶抑制剂苯甲脒（2×10⁻²mol/L）来研究胎盘肽酶对心房利钠肽作用的减弱情况。通过方差分析和配对t检验确定统计学意义。
心房利钠肽和脑利钠肽均能显著减弱对血管紧张素II的血管收缩反应；然而，脑利钠肽更有效。n-硝基-L-精氨酸不影响心房或脑利钠肽对血管紧张素II诱导的血管收缩的减弱作用。在存在苯甲脒的情况下，心房利钠肽发挥出显著更强的血管舒张作用。
与心房利钠肽相比，脑利钠肽是胎盘血管系统更强效的血管舒张剂。心房利钠肽的低效可能与胎盘肽酶有关。一氧化氮不介导心房利钠肽或脑利钠肽的作用。
