Holcberg G, Kossenjans W, Brewer A, Miodovnik M, Myatt L
Department of Obstetrics and Gynecology, University of Cincinnati College of Medicine, OH 45267-0526, USA.
J Soc Gynecol Investig. 1995 Jan-Feb;2(1):1-5.
To determine whether atrial natriuretic peptide (ANP) attenuates the vasoconstrictor effects of angiotensin II (AII), a thromboxane mimetic (U46619), and endothelin-1 in the human fetal-placental vasculature and to determine whether nitric oxide (NO) has a role in the vasodilator activity of ANP.
Isolated placental cotyledons were dually perfused, with fetal perfusion pressure used as an index of vascular response. The effects of AII (10(-10)-10(-6) mol/L bolus injection), endothelin-1 (10(-7) mol/L bolus), and U46619 (10(-9)-10(-6) mol/L bolus or 10(-8) mol/L infusion) were established in the absence or presence of ANP (10(-8) mol/L). The role of NO as a mediator of ANP action was investigated by perfusion with n-nitro-L-arginine (NNLA, 10(-3) mol/L), an inhibitor of NO synthase. Statistical significance was determined by analysis of variance.
Atrial natriuretic peptide caused significant attenuation of vasoconstrictor responses to AII, but weak attenuation of endothelin-1 and no attenuation of U46619. Use of NNLA did not affect the attenuation of AII-induced vasoconstriction by ANP.
Atrial natriuretic peptide is a vasodilator of the fetal-placental vasculature constricted with AII and endothelin-1, but not with U46619. Nitric oxide does not mediate the action of ANP.
确定心房利钠肽（ANP）是否能减弱血管紧张素II（AII）、血栓素类似物（U46619）和内皮素-1在人胎儿-胎盘血管系统中的血管收缩作用，并确定一氧化氮（NO）是否在ANP的血管舒张活性中起作用。
对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ANP（10⁻⁸mol/L）的情况下，确定AII（10⁻¹⁰ - 10⁻⁶mol/L推注）、内皮素-1（10⁻⁷mol/L推注）和U46619（10⁻⁹ - 10⁻⁶mol/L推注或10⁻⁸mol/L输注）的作用。通过用NO合酶抑制剂n-硝基-L-精氨酸（NNLA，10⁻³mol/L）灌注来研究NO作为ANP作用介质的作用。采用方差分析确定统计学意义。
心房利钠肽可显著减弱对AII的血管收缩反应，但对内皮素-1的减弱作用较弱，对U46619无减弱作用。使用NNLA不影响ANP对AII诱导的血管收缩的减弱作用。
心房利钠肽是胎儿-胎盘血管系统的血管舒张剂，对由AII和内皮素-1引起的血管收缩有效，但对U46619引起的血管收缩无效。一氧化氮不介导ANP的作用。
