Renal responses to hypoxemia during renin-angiotensin system inhibition in fetal lambs.
Renal responses to hypoxemia during renin-angiotensin system inhibition in fetal lambs.
复制标题
胎羔肾素-血管紧张素系统抑制期间肾脏对低氧血症的反应。
DOI：
10.1152/ajpregu.1985.249.1.r116
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Robillard,JE
中科院分区：
文献类型：
--
作者：
Nakamura,KT;Ayres,NA;Gomez,RA;Robillard,JE
在长期插管的胎羊（妊娠132-143天;足月145天）中，在给予卡托普利或[Sar 1-Gly 8]ANG II之前和期间，研究了肾素-血管紧张素系统（RAS）在调节低氧血症的肾血流动力学和功能反应中的作用。基线平均动脉血压在给予卡托普利或[Sar 1-Gly 8]ANG II后显著降低。这种降低与卡托普利治疗胎儿的肾血管阻力（RVR）显著下降相关，而在[Sar 1-Gly 8]ANG II治疗胎儿中未观察到RVR变化。然而，肾血流量（RBF）的下降和RVR的上升与低氧血症在对照胎儿中没有减弱显着抑制RAS使用卡托普利或[Sar 1-Gly 8]ANG II。此外，无论是captopril或[Sar 1-Gly 8]ANG II钝化与胎儿低氧血症相关的高血压反应。对卡托普利的肾功能反应与输注[Sar 1-Gly 8]ANG II期间观察到的反应不同。[Sar 1-Gly 8]ANG II的给药可显著降低尿流率（UFR）、肾小球滤过率（GFR）和尿电解质（Na+、K+、Cl-）排泄率，而在卡托普利输注期间未观察到变化。开搏通治疗后低氧血症对肾功能的影响无明显改变。然而，[Sar 1-Gly 8]ANG II倾向于增加UFR和GFR，但这些变化是压力依赖性的，与RAS抑制不直接相关。本研究提示RAS不是低氧血症时胎儿肾脏血流动力学和功能反应的重要介质。
The role of the renin-angiotensin system (RAS) in modulating the renal hemodynamic and functional responses to hypoxemia was studied in chronically catheterized fetal lambs (132-143 days gestation; term 145 days) before and during administration of either captopril or [Sar1-Gly8]ANG II. Base-line mean arterial blood pressure decreased significantly after administration of either captopril or [Sar1-Gly8]ANG II. This decrease was associated with a significant decline in renal vascular resistance (RVR) in captopril-treated fetuses, whereas no changes in RVR were observed in [Sar1-Gly8]ANG II-treated fetuses. However, the decline in renal blood flow (RBF) and the rise in RVR associated with hypoxemia in control fetuses were not attenuated significantly during inhibition of the RAS using either captopril or [Sar1-Gly8]ANG II. Moreover neither captopril nor [Sar1-Gly8]ANG II blunted the hypertensive response associated with fetal hypoxemia. The renal functional response to captopril was different from the response observed during infusion of [Sar1-Gly8]ANG II. Administration of [Sar1-Gly8]ANG II produced significant decreases in urinary flow rate (UFR), glomerular filtration rate (GFR), and urinary electrolyte (Na+, K+, Cl-) excretion rates, whereas no changes were observed during captopril infusion. The effects of hypoxemia on renal function were not modified after captopril. However, [Sar1-Gly8]ANG II tended to increase UFR and GFR, but these changes were pressure-dependent and not directly related to inhibition of the RAS. This study suggests that the RAS is not an important mediator of the fetal renal hemodynamic and functional responses to hypoxemia.