Tissue-specific regulation of type 1 angiotensin II receptor mRNA levels in the rat.
Tissue-specific regulation of type 1 angiotensin II receptor mRNA levels in the rat.
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大鼠 1 型血管紧张素 II 受体 mRNA 水平的组织特异性调节。
DOI：
10.1161/01.hyp.28.3.403
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Schambelan,M
中科院分区：
文献类型：
--
作者：
Sechi,LA;Griffin,CA;Giacchetti,G;Valentin,JP;Llorens-Cortes,C;Corvol,P;Schambelan,M
肾素-血管紧张素系统的大多数生物学效应是由血管紧张素II（Ang II）与1型Ang II（AT 1）受体结合介导的，1型Ang II（AT 1）受体是胎儿生命后存在的主要受体亚型。为了研究大鼠AT 1受体表达的组织特异性调节，我们通过给大鼠喂食低浓度的（0.07% NaCl），正常（0.3% NaCl）或更高（7.5%NaCl）盐饲料14天;输注Ang II（200 ng/kg/min IP）或媒介物7天;和施用血管紧张素转化酶抑制剂（卡托普利，100 mg/dL，在饮用水中）或媒介物7天。用cRNA探针通过狭缝印迹杂交测定肾素、血管紧张素原和总AT 1受体mRNA水平，在cRNA内标存在下通过逆转录聚合酶链反应测定AT 1受体亚型（A和B）。血浆肾素浓度和肾脏肾素，肾脏和肝脏血管紧张素原，和肝脏AT 1受体mRNA水平均呈负相关的盐摄入量，相反，肾脏AT 1受体mRNA水平显着降低，在大鼠喂养低盐，差异是完全由于AT 1A亚型减少。这种差异似乎并不介导的血管紧张素II的循环水平的变化，因为血管紧张素II输注降低血浆肾素浓度和肾肾素mRNA的血管紧张素原或AT 1受体mRNA水平在肾脏或肝脏没有影响;肾血管紧张素II受体密度（由原位放射自显影测定）下降，推测通过转录后机制。同样地，用卡托普利抑制Ang II的生成，可增加血浆肾素浓度和肾肾素mRNA水平，而不改变肾或肝血管紧张素原mRNA或肾AT 1受体mRNA水平。因此，AT 1受体基因表达的组织特异性的方式，是不同于其他组件的系统和本地的肾素-血管紧张素系统，似乎是通过一种机制，而不是通过血管紧张素II的循环水平的变化介导的。
Most of the biological effects of the renin-angiotensin system are mediated by the binding of angiotensin II (Ang II) to the type 1 Ang II (AT1) receptor, the predominant receptor subtype present after fetal life. To study tissue-specific regulation of the expression of the AT1receptor in the rat, we altered activity of the renin-angiotensin system by feeding rats a low (0.07% NaCl), normal (0.3% NaCl), or high (7.5% NaCl) salt chow for 14 days; infusing Ang II (200 ng/kg per minute IP) or vehicle for 7 days; and administering an angiotensin-converting enzyme inhibitor (captopril, 100 mg/dL in the drinking water) or vehicle for 7 days. Renin, angiotensinogen, and total AT1receptor mRNA levels were measured by slot-blot hybridization with cRNA probes, and AT1receptor subtypes (A and B) were measured by reverse transcription–polymerase chain reaction in the presence of a cRNA internal standard. Plasma renin concentration and renal renin, renal and hepatic angiotensinogen, and hepatic AT1receptor mRNA levels were all inversely related to salt intake; in contrast, renal AT1receptor mRNA levels were significantly lower in rats fed low salt, a difference that was exclusively due to a decrease in the AT1Asubtype. This difference did not appear to be mediated by a change in the circulating levels of Ang II, because Ang II infusion reduced plasma renin concentration and renal renin mRNA with no effect on either angiotensinogen or AT1receptor mRNA levels in kidney or liver; renal Ang II receptor density (determined by in situ autoradiography) decreased, presumably via a posttranscriptional mechanism. Similarly, inhibition of Ang II generation with captopril increased plasma renin concentration and renal renin mRNA levels without altering renal or hepatic angiotensinogen mRNA or renal AT1receptor mRNA levels. Thus, AT1receptor gene expression is regulated in a tissue-specific manner that is distinct from other components of systemic and local renin-angiotensin systems and that appears to be mediated by a mechanism other than through changes in the circulating levels of Ang II.
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大鼠心脏中心脏血管紧张素II AT1受体基因的表达受类固醇调节，但不受血管紧张素II调节
影响因子：
4.9
作者：
R. Bruna;Stefan Ries;Carola Himmelstoss;A. Kurtz
通讯作者：
A. Kurtz
DOI：
10.1016/0006-291x(92)91844-g
发表时间：
1992-02-14
影响因子：
3.1
作者：
IWAI, N;INAGAMI, T
通讯作者：
INAGAMI, T
大鼠 1 型血管紧张素 II 受体基因表达的个体发育。
DOI：
10.1172/jci116232
发表时间：
1993
期刊：
The Journal of clinical investigation
影响因子：
--
作者：
Tufro-McReddie,A;Harrison,JK;Everett,AD;Gomez,RA
通讯作者：
Gomez,RA
低钠饮食对大鼠肾脏血管紧张素 II 受体亚型的差异调节。
DOI：
10.1161/01.hyp.25.4.872
发表时间：
1995
期刊：
Hypertension (Dallas, Tex. : 1979)
影响因子：
--
作者：
Du,Y;Yao,A;Guo,D;Inagami,T;Wang,DH
通讯作者：
Wang,DH
链脲佐菌素诱导的大鼠糖尿病中的肾素-血管紧张素系统。
DOI：
10.1681/asn.v461337
发表时间：
1993
期刊：
Journal of the American Society of Nephrology : JASN
影响因子：
--
作者：
Kalinyak,JE;Sechi,LA;Griffin,CA;Don,BR;Tavangar,K;Kraemer,FB;Hoffman,AR;Schambelan,M
通讯作者：
Schambelan,M