Role of the renin-angiotensin system in hypertension during reduced uteroplacental perfusion pressure.
Role of the renin-angiotensin system in hypertension during reduced uteroplacental perfusion pressure.
复制标题
肾素-血管紧张素系统在子宫胎盘灌注压降低期间高血压中的作用。
DOI：
10.1152/ajpregu.1989.257.1.r204
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Brooks,VL
中科院分区：
文献类型：
--
作者：
Woods,LL;Brooks,VL
已知子宫-胎盘缺血可引起各种物种的全身性高血压，但其机制尚不清楚。这些研究旨在验证这样一种假设，即在子宫胎盘灌注压降低期间发生的体动脉压升高是由肾素-血管紧张素系统介导的，可能是由于缺血妊娠子宫释放肾素或血管紧张素所致。在训练有素、长期使用器械的怀孕犬(孕龄47+/-2天，足月=60天)中，维持正常的Na+摄入量(约80meq/天)，通过放置在肾动脉远端但子宫动脉近端的充气主动脉封堵器将子宫灌流压降至60 mm Hg，并以此水平伺服控制1h。体动脉压上升14+/-2 mm Hg，从96+/-7升至110+/-8 mm Hg。血浆肾素活性和血管紧张素II水平无明显变化。在同一动物的另一天，通过输注卡托普利和足够的血管紧张素II使动脉压恢复到正常(2-5ng.kg-1.min-1静脉注射)来固定肾素-血管紧张素系统的活性。在肾素-血管紧张素系统不变的情况下，将子宫动脉压降低到60毫米汞柱可使体循环动脉压升高10+/-2毫米汞柱，这一反应与对照实验中的反应没有什么不同。这些数据表明，子宫胎盘灌流压降低时体循环动脉压升高与肾素-血管紧张素系统无关。
Utero-placental ischemia is known to cause systemic hypertension in various species, but the mechanisms are unknown. These studies were designed to test the hypothesis that the increased systemic arterial pressure that occurs during reduced utero-placental perfusion pressure is mediated by the renin-angiotensin system, possibly due to release of renin or angiotensin from the ischemic gravid uterus. In trained, chronically instrumented pregnant dogs (gestational age 47 +/- 2 days, term = 60 days) maintained on a normal Na+ intake (approximately 80 meq/day), uterine perfusion pressure was reduced to 60 mmHg with an inflatable aortic occluder positioned distal to the renal arteries but proximal to the uterine arteries and was servo-controlled at this level for 1 h. Systemic arterial pressure rose by 14 +/- 2 mmHg, from 96 +/- 7 to 110 +/- 8 mmHg. Plasma renin activity and angiotensin II levels did not change significantly. On another day in the same animals, the activity of the renin-angiotensin system was fixed by infusing captopril and sufficient angiotensin II to restore arterial pressure to normal (2-5 ng.kg-1.min-1 iv). Reduction of uterine artery pressure to 60 mmHg caused systemic arterial pressure to increase by 10 +/- 2 mmHg with the renin-angiotensin system fixed, a response not different from that in the control experiments. These data suggest that the increase in systemic arterial pressure during reduced uteroplacental perfusion pressure is independent of the renin-angiotensin system.