Homeostasis in mice with genetically decreased angiotensinogen is primarily by an increased number of renin-producing cells

被引:55
作者
Kim, HS [1 ]
Maeda, N
Oh, GT
Fernandez, LG
Gomez, RA
Smithies, O
机构
[1] Univ N Carolina, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA
[2] Univ Virginia, Hlth Sci Ctr, Dept Pediat, Charlottesville, VA 22908 USA
关键词
D O I
10.1074/jbc.274.20.14210
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:14210 / 14217
页数:8
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