Moore L C, Casellas D
Department of Physiology and Biophysics, State University of New York, Stony Brook.
Kidney Int. 1990 Jun;37(6):1402-8. doi: 10.1038/ki.1990.129.
Experiments were performed in blood-perfused juxtamedullary nephrons in vitro to evaluate the tubuloglomerular feedback (TGF) dependence of autoregulatory vasoconstriction in mid-to-late (mAA) and juxtaglomerular (jAA) afferent arterioles. Videometric measurements were made of perfusion pressure (PP) dependent changes in lumen diameter of superficial vessels before and after acute inhibition of the TGF mechanism by direct microinfusion of 0.1 mM furosemide solution into the macula densa (MD) segment. When PP was raised from 60 to 123 +/- 7 mm Hg in seven vessels, jAA diameter decreased by 29 +/- 3% (SEM, N = 7). During furosemide infusion with the same change in PP, jAA diameter decreased only 7 +/- 2%. After calcium channel blockade with 1 micromolar nimodipine, jAA lumen diameter increased by 21 +/- 7%. A similar pattern of responses was observed in eight jAA where TGF was inhibited with an oil block at the MD. mAA autoregulatory responses were also blunted by TGF inhibition. Raising PP from 60 to 120 mm Hg resulted in 15 +/- 2% and 7 +/- 2% decreases in mAA luminal diameter before and after TGF inhibition. These results demonstrate that the autoregulatory responses in mid- and juxtaglomerular afferent arteriolar segments are mediated by both TGF and a TGF-independent myogenic mechanism.
在体外对血液灌注的近髓肾单位进行实验，以评估中晚期（mAA）和球旁（jAA）传入小动脉自身调节性血管收缩对肾小管-肾小球反馈（TGF）的依赖性。通过将0.1 mM速尿溶液直接微量注入致密斑（MD）段急性抑制TGF机制前后，对浅表血管管腔直径随灌注压（PP）变化进行视频测量。当7个血管的PP从60升高到123±7 mmHg时，jAA直径下降29±3%（SEM，N = 7）。在速尿输注期间，PP有相同变化时，jAA直径仅下降7±2%。用1微摩尔尼莫地平阻断钙通道后，jAA管腔直径增加21±7%。在8个通过MD处油块抑制TGF的jAA中观察到类似的反应模式。TGF抑制也使mAA自身调节反应减弱。将PP从60升高到120 mmHg，在TGF抑制前后，mAA管腔直径分别下降15±2%和7±2%。这些结果表明，中晚期和球旁传入小动脉段的自身调节反应由TGF和一种不依赖TGF的肌源性机制介导。
