Abolished tubuloglomerular feedback and increased plasma renin in adenosine A1 receptor-deficient mice
Abolished tubuloglomerular feedback and increased plasma renin in adenosine A1 receptor-deficient mice
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DOI：
10.1152/ajpregu.00470.2001
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发表时间：
2001-11-01
影响因子：
2.8
通讯作者：
Persson, AEG
中科院分区：
文献类型：
--
作者：
Brown, R;Ollerstam, A;Persson, AEG
利用A(1)R敲除小鼠验证腺苷作用于腺苷A(1)受体（A(1)R）调节多种肾功能并介导小管肾小球反馈（TGF）的假说。我们麻醉敲除小鼠、野生型小鼠和杂合子小鼠，并测量肾小球滤过率、TGF反应（使用停止流压（Psf）技术）和血浆肾素浓度。与野生型和杂合子小鼠相比，A(1)R基因敲除小鼠的血压升高。所有基因型的肾小球滤过率相似。A(1)R+/+小鼠近端肾小管P-sf从36.7 +/- 1.2降低到25.3 +/- 1.6 mmHg， A(1)R+/-小鼠近端肾小管P-sf从38.1 +/- 1.0降低到27.4 +/- 1.1 mmHg。这种反应在纯合子A(1)R-/-小鼠（从39.1 +/- 4.1到39.2 +/- 4.5 mmHg）中消失。A(1)R基因敲除小鼠血浆肾素活性[74.2 +/- 14.3 mGU/ml]显著高于野生型和A(1)R基因敲除小鼠（36.3 +/- 8.5和34.1 +/- 9.6 mGU/ml）。结果表明，腺苷作用于A(1)R是TGF必需的，并调节肾素释放。
The hypothesis that adenosine acting on adenosine A(1) receptors (A(1)R) regulates several renal functions and mediates tubuloglomerular feedback (TGF) was examined using A(1)R knockout mice. We anesthetized knockout, wild-type, and heterozygous mice and measured glomerular filtration rate, TGF response using the stop-flow pressure (Psf) technique, and plasma renin concentration. The A(1)R knockout mice had an increased blood pressure compared with wild-type and heterozygote mice. Glomerular filtration rate was similar in all genotypes. Proximal tubular P-sf was decreased from 36.7 +/- 1.2 to 25.3 +/- 1.6 mmHg in the A(1)R+/+ mice and from 38.1 +/- 1.0 to 27.4 +/- 1.1 mmHg in A(1)R+/- mice in response to an increase in tubular flow rate from 0 to 35 nl/min. This response was abolished in the homozygous A(1)R-/- mice (from 39.1 +/- 4.1 to 39.2 +/- 4.5 mmHg). Plasma renin activity was significantly greater in the A(1)R knockout mice [74.2 +/- 14.3 milli-Goldblatt units (mGU)/ml] mice compared with the wild-type and A(1)R+/- mice (36.3 +/- 8.5 and 34.1 +/- 9.6 mGU/ml), respectively. The results demonstrate that adenosine acting on A(1)R is required for TGF and modulates renin release.