Abnormal regulation of proximal tubule renin mRNA in the Dahl/Rapp salt-sensitive rat.
Abnormal regulation of proximal tubule renin mRNA in the Dahl/Rapp salt-sensitive rat.
复制标题
Dahl/Rapp 盐敏感大鼠中近端小管肾素 mRNA 的异常调节。
DOI：
10.1046/j.1523-1755.1998.00160.x
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Henrich,WL
中科院分区：
文献类型：
--
作者：
Tank,JE;Moe,OW;Henrich,WL
Dahl/Rapp盐敏感大鼠近端小管肾素mRNA的异常调节。BackgroundThe precise pathogenesis of salt-sensitive hypertension in the Dahl rat is unknown. abbably在肾血流动力学和氯化钠处理已牵连，并可能涉及到的活动的intrarrenal肾素-血管紧张素system.MethodsCirculating，aptaglomerular和intrarrenal（肾小球和近端肾小管）的肾素的变化进行了研究，在达尔/拉普盐敏感和耐盐大鼠喂养与正常（0.5%）或高（4%）氯化钠饮食。通过测量血浆肾素活性和肾素分泌率来评估循环和肾小球中的肾素。采用显微切割和定量竞争性RT-PCR方法检测大鼠肾小球和近端肾小管中的肾素mRNA水平。结果高盐饮食可抑制高盐敏感大鼠的循环和肾小球中的肾素水平（血浆肾素活性0.5%，10.9 ± 0.7vs.4%，7.9 ± 0.3ng/ml/hr，P< 0.05;肾素分泌率0.5% 220 ± 32vs.4%，58 ± 5 ng/mg/hr，P< 0.05）。高盐饮食也抑制了盐敏感动物的肾小球肾素mRNA表达（0.5%，411 ± 84vs.4%，67 ± 22 × 103拷贝/肾小球，P< 0.05）。相反，在盐敏感动物中，高NaCl饮食不会抑制近端肾小管肾素（0.5%，13.9 ± 2.7vs.4%，12.1 ± 3.6 × 103拷贝/mm小管，P= NS），但在耐盐大鼠中受到抑制（0.5%，9.5 ± 2.8vs.4%，3.2 ± 1.2 × 103 copies/mm，P< 0.05）.结论高盐饮食不能抑制近端肾小管肾素可能导致局部血管紧张素II生成增加和近端肾小管对NaCl的吸收增加，从而导致盐敏感性高血压的产生。
Abnormal regulation of proximal tubule renin mRNA in the Dahl/Rapp salt-sensitive rat.BackgroundThe precise pathogenesis of salt-sensitive hypertension in the Dahl rat is unknown. Abnormalities in renal hemodynamics and NaCl handling have been implicated, and may relate to changes in the activity of the intrarenal renin-angiotensin system.MethodsCirculating, juxtaglomerular and intrarenal (glomerular and proximal tubular) renin were studied in Dahl/Rapp salt-sensitive and salt-resistant rats fed with a normal (0.5%) or high (4%) NaCl diet. Circulating and juxtaglomerular renin were assessed by measurement of plasma renin activity and renin secretory rates. Glomerular and proximal tubular renin mRNA were assessed by microdissection and quantitative competitive RT-PCR.ResultsCirculating and juxtaglomerular renin were suppressed by high dietary NaCl in salt-sensitive rats (plasma renin activity, 0.5%, 10.9 ± 0.7 vs. 4%, 7.9 ± 0.3 ng/ml/hr,P< 0.05; renin secretory rate, 0.5% 220 ± 32 vs. 4%, 58 ± 5 ng/mg/hr,P< 0.05). Glomerular renin mRNA was also suppressed by the higher salt diet in salt-sensitive animals (0.5%, 411 ± 84 vs. 4%, 67 ± 22 × 103copies/glomerulus,P< 0.05). In contrast, proximal tubular renin was not suppressed by a high NaCl diet in salt-sensitive animals (0.5%, 13.9 ± 2.7 vs. 4%, 12.1 ± 3.6 × 103copies/mm tubule,P= NS), but was suppressed in salt-resistant rats (0.5%, 9.5 ± 2.8 vs. 4%, 3.2 ± 1.2 × 103copies/mm,P< 0.05).ConclusionsFailure to suppress proximal tubular renin in response to high dietary NaCl may result in increased local generation of angiotensin II and enhanced proximal tubular NaCl absorption, and thereby contribute to the generation of salt sensitive hypertension.