Normotensive blood pressure in mice with a disrupted renin Ren-1(d) gene

被引:9
作者
Bertaux, F
Colledge, WH
Smith, SE
Evans, M
Samani, NJ
Miller, CCJ
机构
[1] INST PSYCHIAT,DEPT NEUROL,LONDON SE5 8AF,ENGLAND
[2] UNIV CAMBRIDGE,DEPT PHYSIOL,CAMBRIDGE CB2 3EG,ENGLAND
[3] CRC,WELLCOME INST CANC & DEV BIOL,CAMBRIDGE CB2 1QR,ENGLAND
[4] UNIV LEICESTER,DEPT CARDIOL,LEICESTER LE3 9QP,LEICS,ENGLAND
关键词
renin; renin angiotensin system; blood pressure;
D O I
10.1023/A:1018438023675
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
Renin is an aspartyl protease that is involved in the conversion of angiotensinogen to angitensin II and hence participates in ihs regulation of blood pressure. Mice are polymorphic for the number of renin genes with some strains harbouring two renin genes, Ren-1(d) and Ren-2. To study the role of renin Ren-1(d) in regulating cardiovascular homeostasis, mice with a disrupted Ren-1(d) gene were created. Analyses of kidney renin mRNA expression in Ren-1(d-/-)/Ren-(2+/+) mice demonstrated that only Ren-2 transcripts were present. Mean arterial blood pressures of Ren-1(d+/+)/Ren-2(+/+), Ren-1d(+/-)/Ren-2(+/+) and Ren-1(d-/-)/Ren-2(+/+) mice showed no significant differences. These observations demonstrate that the Ren-1(d) gene product is not essential for normal blood pressure maintenance under normal physiological conditions.
引用
收藏
页码:191 / 196
页数:6
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