Interactions between adenosine and angiotensin II in controlling glomerular filtration.
Interactions between adenosine and angiotensin II in controlling glomerular filtration.
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腺苷和血管紧张素 II 在控制肾小球滤过方面的相互作用。
DOI：
10.1152/ajprenal.1985.248.3.f340
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Hester,RL
中科院分区：
文献类型：
--
作者：
Hall,JE;Granger,JP;Hester,RL
本研究探讨腺苷（Ado）和血管紧张素II（ANG II）在控制肾血流量（RBF）和肾小球滤过率（GFR）中的相互作用。在6只正常犬中，肾内注射Ado（1.0 mumol/min）可短暂降低RBF，但在持续注射Ado期间，RBF增加至对照组的122 +/- 7%，尽管GFR仍为对照组的75 +/- 6%。用转换酶抑制剂SQ 14225阻断ANG II的形成（n = 6）几乎消除了RBF的短暂下降，但不能阻止Ado引起的GFR的持续下降。当通过静脉输注SQ 14225和20 ng保持循环ANG II恒定时。kg-1 . min ~（-1）的ANG Ⅱ（n = 6），Ado使RBF一过性下降，但恢复较正常犬慢，且RBF无明显升高。维持恒定的循环血管紧张素II并不能阻止肾小球滤过率的下降。这些观察结果表明，血管紧张素Ⅱ介导的GFR降低并不完全依赖于血管紧张素Ⅱ，可能是由于阿多扩张传出小动脉。然而，短暂的肾血管收缩所造成的Ado依赖于血管紧张素II，从这项研究的数据表明，部分衰减收缩反应Ado是由于抑制肾素分泌和内源性血管紧张素II的形成。在维持高ANG II水平的情况下（即，缺血性肾衰竭），Ado可能能够引起持续的肾血管收缩。
This study examined interactions between adenosine (Ado) and angiotensin II (ANG II) in controlling renal blood flow (RBF) and glomerular filtration rate (GFR). In six normal dogs, intrarenal Ado infusion (1.0 mumol/min) transiently decreased RBF, but during sustained Ado infusion RBF increased to 122 +/- 7% of control, although GFR remained at 75 +/- 6% of control. Blockade of ANG II formation with the converting enzyme inhibitor SQ 14225 (n = 6) almost abolished the transient decrease in RBF but did not prevent the sustained fall in GFR caused by Ado. When circulating ANG II was held constant by intravenous infusion of SQ 14225 and 20 ng . kg-1 . min-1 of ANG II (n = 6), Ado transiently decreased RBF but the return of RBF was much slower than in normal dogs and RBF did not increase above control. Maintenance of constant circulating ANG II did not prevent Ado-mediated decreases in GFR. These observations suggest that Ado-mediated reductions in GFR do not depend entirely on ANG II and may be due to dilation of efferent arterioles by Ado. However, the transient renal vasoconstriction caused by Ado depends on ANG II, and data from this study suggest that part of the waning constrictor response to Ado is due to suppression of renin secretion and endogenous ANG II formation. In circumstances where high ANG II levels are maintained (i.e., ischemic renal failure), Ado may be capable of causing sustained renal vasoconstriction.