Huang W C, Bell P D, Harvey D, Mitchell K D, Navar L G
Nephrology Research and Training Center, University of Alabama, Birmingham.
Kidney Int. 1988 Nov;34(5):631-7. doi: 10.1038/ki.1988.227.
The tubuloglomerular feedback (TGF) mechanism was evaluated in the nonclipped kidney of Goldblatt hypertensive rats from both stop flow pressure (SFP) and single nephron glomerular filtration rate (SNGFR) responses to step increases in late proximal perfusion rate from 0 to 40 nl/min. During control conditions, increases in late proximal perfusion rate produced flow dependent decreases in SFP and SNGFR with maximal values of 10.2 +/- 1.0 mm Hg and 12.9 +/- 2.5 nl/min, values similar to those obtained in normal rats. During ACE inhibition (MK 422; 0.6 mg/kg/hr), arterial pressure decreased from 168 +/- 8 to 137 +/- 7 mm Hg and there was a marked attenuation in the magnitude of SFP feedback responses (delta = 2.5 +/- 0.3 mm Hg). SNGFR feedback responses, however, were not significantly impaired. Direct decreases in renal arterial pressure reduced control SFP but SFP feedback responses were maintained, indicating that the attenuated SFP feedback responses during ACE inhibition were not due to decreased arterial pressure. Superimposed infusion of angiotensin II during ACE inhibition partially restored SFP feedback responses. In contrast, norepinephrine infusion did not result in a similar restoration of SFP feedback sensitivity. These results indicate that the nonclipped kidney of Goldblatt hypertensive rats has an intact TGF mechanism as assessed from SFP and SNGFR feedback responses. Furthermore, ACE inhibition attenuates SFP but not SNGFR feedback responses, and systemic angiotensin II infusions can restore SFP feedback responsiveness towards normal.
从肾血流量停止时的压力（SFP）和单肾单位肾小球滤过率（SNGFR）对近端肾小管灌注速率从0至40 nl/min逐步增加的反应，评估了Goldblatt高血压大鼠非夹闭肾的球管反馈（TGF）机制。在对照条件下，近端肾小管灌注速率增加导致SFP和SNGFR呈流量依赖性降低，最大值分别为10.2±1.0 mmHg和12.9±2.5 nl/min，这些值与正常大鼠所获得的值相似。在血管紧张素转换酶（ACE）抑制期间（MK 422；0.6 mg/kg/小时），动脉压从168±8 mmHg降至137±7 mmHg，SFP反馈反应的幅度显著减弱（δ=2.5±0.3 mmHg）。然而，SNGFR反馈反应并未受到显著损害。肾动脉压直接降低会降低对照SFP，但SFP反馈反应得以维持，这表明ACE抑制期间SFP反馈反应减弱并非由于动脉压降低所致。在ACE抑制期间叠加输注血管紧张素II可部分恢复SFP反馈反应。相比之下，输注去甲肾上腺素并未导致SFP反馈敏感性出现类似恢复。这些结果表明，从SFP和SNGFR反馈反应评估，Goldblatt高血压大鼠的非夹闭肾具有完整的TGF机制。此外，ACE抑制可减弱SFP而非SNGFR反馈反应，全身性输注血管紧张素II可使SFP反馈反应性恢复至正常。
