Huang W C, Navar L G
Department of Physiology and Biophysics, National Defense Medical Center, Taipei, Taiwan, Republic of China.
Proc Natl Sci Counc Repub China B. 1988 Jul;12(3):180-5.
To examine the modulatory role of angiotensin II on the tubuloglomerular feedback (TGF) mechanism, TGF responses were assessed during control conditions, converting enzyme inhibition (CEI; MK 422, 0.6 mg/kg.hr) and during continued CEI with the replacement of angiotensin II. TGF responses were assessed from stop flow pressure (SFP) feedback responses obtained during step increases in the late proximal perfusion rate from 0-40 nl/min. SFP values in the absence of perfusion were used to estimate glomerular pressure (GP) under conditions where the influence of the TGF mechanism should be at a minimum. During CEI, the arterial pressure decreased from 124 +/- 3 to 106 +/- 3 mmHg and the estimated GP decreased from 53 +/- 1.4 to 49 +/- 0.8 mmHg. There was a marked attenuation in the magnitude of SFP feedback responses from 11.0 +/- 1.3 to 2.7 +/- 0.6 mmHg. TGF feedback responses, however, were restored towards normal during superimposed angiotensin II infusion (7.7 +/- 0.9 mmHg). These results indicate that converting enzyme inhibition decreases the effects of angiotensin II on the kidney through TGF dependent mechanism.
为研究血管紧张素II对肾小管-肾小球反馈（TGF）机制的调节作用，在对照条件下、转换酶抑制（CEI；MK 422，0.6毫克/千克·小时）期间以及持续CEI并补充血管紧张素II的过程中评估了TGF反应。通过在近曲小管晚期灌注速率从0至40纳升/分钟逐步增加期间获得的停流压力（SFP）反馈反应来评估TGF反应。在不存在灌注的情况下的SFP值用于估计在TGF机制影响应最小的条件下的肾小球压力（GP）。在CEI期间，动脉压从124±3降至106±3毫米汞柱，估计的GP从53±1.4降至49±0.8毫米汞柱。SFP反馈反应的幅度从11.0±1.3显著衰减至2.7±0.6毫米汞柱。然而，在叠加血管紧张素II输注期间（7.7±0.9毫米汞柱），TGF反馈反应恢复至正常。这些结果表明，转换酶抑制通过TGF依赖性机制降低血管紧张素II对肾脏的作用。
