Morsing P, Persson A E
Department of Physiology and Biophysics, University of Lund, Sweden.
Am J Physiol. 1991 Jun;260(6 Pt 2):F868-73. doi: 10.1152/ajprenal.1991.260.6.F868.
The role of bradykinin in resetting the tubuloglomerular feedback (TGF) mechanism was studied with the stop-flow technique in control and hydronephrotic Inactin-anesthetized rats. Glomerular function was assessed by measuring stop-flow pressure (Psf); the maximal decrease in stop-flow pressure (delta Psf) with increased loop of Henle perfusion and the perfusion that elicited half-maximal delta Psf, the turning point (TP), were determined. Bradykinin infusion resulted in resetting of TGF in both control and hydronephrotic rats but in different directions. A decreased sensitivity was found in control rats (TP increased from 18.6 to 26.4 and 16.8 to 22.1 nl/min on systemic and intratubular administration, respectively). In hydronephrotic rats the sensitivity of TGF increased. TP decreased from 19.9 to 15.2 nl/min with bradykinin administered systemically and from 18.4 to 15.0 nl/min on intratubular administration. These results show that exogenous kinin administration mimics the effects of extracellular volume expansion on TGF resetting and demonstrate a difference in resetting in hydronephrotic and control kidneys.
采用停流技术，在对照和肾积水的因纳克麻醉大鼠中研究了缓激肽在重置肾小管-肾小球反馈（TGF）机制中的作用。通过测量停流压力（Psf）评估肾小球功能；确定随着髓袢灌注增加停流压力的最大降低值（ΔPsf）以及引起半最大ΔPsf的灌注量即转折点（TP）。缓激肽输注导致对照和肾积水大鼠的TGF均发生重置，但方向不同。在对照大鼠中发现敏感性降低（全身给药时TP从18.6增加到26.4 nl/min，肾小管内给药时从16.8增加到22.1 nl/min）。在肾积水大鼠中，TGF的敏感性增加。全身给予缓激肽时TP从19.9降至15.2 nl/min，肾小管内给药时从18.4降至15.0 nl/min。这些结果表明，外源性激肽给药模拟了细胞外液量扩张对TGF重置的影响，并证明了肾积水肾脏和对照肾脏在重置方面的差异。
