肾动脉输注血管紧张素I对钠负荷充足犬肾小球动力学的影响。

Effects of renal arterial angiotensin I infusion on glomerular dynamics in sodium replete dogs.

作者信息

Rosivall L, Carmines P K, Navar L G

出版信息

Kidney Int. 1984 Sep;26(3):263-8. doi: 10.1038/ki.1984.168.

DOI:10.1038/ki.1984.168

Abstract

During intrarenal infusion of angiotensin I (AI), conversion to angiotensin II (AII) within the kidney has been shown to occur early enough to decrease glomerular filtration rate (GFR). To evaluate further the mechanism by which AI decreases GFR, micropuncture studies were conducted in sodium replete dogs. Feedback-mediated alterations in glomerular function were minimized by reducing renal arterial pressure to 90 mm Hg. During infusion of AI (0.82 +/- 0.01 micrograms min-1), renal blood flow (3.91 +/- 0.25 ml min-1 g-1) and GFR (0.63 +/- 0.04 ml min-1 g-1) decreased by 36.7 +/- 6.1% and 18.9 +/- 6.1%, respectively. Similarly, single nephron GFR decreased from 66.4 +/- 3.8 to 40.0 +/- 3.2 nl min-1 and estimated glomerular plasma flow (280 +/- 49 nl min-1) decreased by 55 +/- 6%. Stop-flow pressure (40.5 +/- 3.6 mm Hg) did not change significantly, while proximal tubular (21.8 +/- 1.4 mm Hg) and peritubular capillary pressures (13.2 +/- 1.8 mm Hg) decreased by 25.5 +/- 2.8% and 49.4% +/- 5.1%, respectively. Glomerular capillary and effective filtration pressures were not altered significantly. There were increases in both preglomerular (168%) and efferent (203%) arteriolar resistances, along with a decrease in the glomerular filtration coefficient (Kf) from 4.6 +/- 0.6 to 2.5 +/- 0.5 nl mm Hg-1 min-1. These data indicate that augmented intrarenal conversion of circulating AI reduces GFR as a consequence of decreases in Kf as well as in glomerular plasma flow, the latter being due to concomitant increases in preglomerular and efferent arteriolar resistances.

摘要

在肾内输注血管紧张素I（AI）期间，已表明在肾脏内转化为血管紧张素II（AII）发生得足够早，足以降低肾小球滤过率（GFR）。为了进一步评估AI降低GFR的机制，在钠充足的犬身上进行了微穿刺研究。通过将肾动脉压降至90 mmHg，使反馈介导的肾小球功能改变最小化。在输注AI（0.82±0.01微克·分钟⁻¹）期间，肾血流量（3.91±0.25毫升·分钟⁻¹·克⁻¹）和GFR（0.63±0.04毫升·分钟⁻¹·克⁻¹）分别下降了36.7±6.1%和18.9±6.1%。同样，单个肾单位GFR从66.4±3.8降至40.0±3.2纳升·分钟⁻¹，估计肾小球血浆流量（280±49纳升·分钟⁻¹）下降了55±6%。停流压力（40.5±3.6 mmHg）无显著变化，而近端肾小管压力（21.8±1.4 mmHg）和肾小管周围毛细血管压力（13.2±1.8 mmHg）分别下降了25.5±2.8%和49.4%±5.1%。肾小球毛细血管压力和有效滤过压无显著改变。肾小球前（168%）和出球（203%）小动脉阻力均增加，同时肾小球滤过系数（Kf）从4.6±0.6降至2.5±0.5纳升·毫米汞柱⁻¹·分钟⁻¹。这些数据表明，循环AI在肾内的转化增强导致GFR降低，这是由于Kf以及肾小球血浆流量降低所致，后者是由于肾小球前和出球小动脉阻力同时增加所致。