Homeostasis in mice with genetically decreased angiotensinogen is primarily by an increased number of renin-producing cells
Homeostasis in mice with genetically decreased angiotensinogen is primarily by an increased number of renin-producing cells
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DOI：
10.1074/jbc.274.20.14210
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发表时间：
1999-05-14
影响因子：
4.8
通讯作者：
Smithies, O
中科院分区：
文献类型：
--
作者：
Kim, HS;Maeda, N;Smithies, O
在这里，我们研究了一个血管紧张素原基因失活的小鼠肾素-血管紧张素系统内分泌分支中发生的血压稳态的生化、分子和细胞变化。在血管紧张素原合成的主要组织肝脏中，剩余的正常等位基因没有代偿性上调。编码血管紧张素转换酶或血管紧张素主要压力调节受体的基因的表达没有显著变化，但只有一个血管紧张素原基因拷贝的小鼠血浆肾素浓度是野生型的两倍多。这种增加主要是由于肾小球近肾小球器官中产生肾素的比例适度增加，以及肾小球传入小动脉中产生肾素的细胞数量是野生型肾素细胞数量的四倍，而不是由于已经致力于合成肾素的细胞中肾素产量的上调。
Here we investigate the biochemical, molecular, and cellular changes directed toward blood pressure homeostasis that occur in the endocrine branch of the renin-angiotensin system of mice having one angiotensinogen gene inactivated. No compensatory up-regulation of the remaining normal allele occurs in tbe liver, the main tissue of angiotensinogen synthesis. No significant changes occur in expression of the genes coding for the angiotensin converting enzyme or the major pressor-mediating receptor for angiotensin, but plasma renin concentration in the mice having only one copy of the angiotensinogen gene is greater than twice wild-type, This increase is mediated primarily by a modest increase in the proportion of renal glomeruli producing renin in their juxtaglomerular apparatus and by four times wild-type numbers of renin-producing cells along afferent arterioles of the glomeruli rather than by upregulating renin production in cells already committed to its synthesis.