卡托普利对人胎儿胎盘循环中缓激肽失活的影响。
Effect of captopril on bradykinin inactivation by human foetal placental circulation.
作者信息
Soares de Moura R, Solano Vale N
出版信息
Br J Clin Pharmacol. 1986 Feb;21(2):143-8. doi: 10.1111/j.1365-2125.1986.tb05168.x.
The inactivation of bradykinin on passage across the human foetal placental circulation was investigated in six full-term human placentas. The placentas were perfused with a modified Krebs-Henseleit solution and placenta perfusion pressure was recorded. Samples collected at the arterial inflow and at the venous effluent were assayed on the isolated guinea-pig ileum as an estimation of bradykinin activity. Bradykinin (100 ng ml-1) was infused through the foetal placental vessels before and during captopril 4 X 10(-7) M. Bradykinin produced a transient increase in placental vascular resistance that was not potentiated by captopril. Bradykinin activity was completely abolished after passage through the foetal placental circulation, and the inactivation was blocked by captopril. These data suggest that angiotensin I converting enzyme (kininase II) might occur in the foetal placental vessels.
在六个足月的人胎盘上研究了缓激肽在通过人胎儿胎盘循环时的失活情况。用改良的克雷布斯-亨泽莱特溶液灌注胎盘，并记录胎盘灌注压力。在动脉流入处和静脉流出处采集的样本在离体豚鼠回肠上进行测定，以估计缓激肽活性。在卡托普利4×10⁻⁷M之前和期间，通过胎儿胎盘血管注入缓激肽（100 ng/ml⁻¹）。缓激肽使胎盘血管阻力短暂增加，卡托普利并未增强这种作用。缓激肽活性在通过胎儿胎盘循环后完全消失，且这种失活被卡托普利阻断。这些数据表明，血管紧张素I转换酶（激肽酶II）可能存在于胎儿胎盘血管中。
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