The use of designer rats in the genetic dissection of hypertension

被引：30
作者：
Kwitek-Black A.E. [1 ]
Jacob H.J. [1 ]
机构：
[1] Department of Physiology, Human Molecular Genetics Center, Medical College of Wisconsin, Milwaukee, WI
来源：
Current Hypertension Reports | 2001年 / 3卷 / 1期
关键词：
Quantitative Trait Locus; Quantitative Trait Locus Region; Congenic Strain; Recipient Strain; Donor Strain;
D O I：
10.1007/s11906-001-0072-0
中图分类号：
学科分类号：
摘要：
The rat is a well-established model for hypertension research, in both physiologic and pharmacologic study. Quantitative trait loci (QTL) for blood pressure and related phenotypes have been described on every rat chromosome; therefore, more simplified models must be generated to identify and study the function of the gene(s) located by QTL analysis. Designer rat strains, such as congenic and consomic strains, which share phenotypic and genotypic characteristics with humans but with a greatly simplified genetic background, would yield a powerful platform for functional studies, especially when combined with microarray technologies. Development of these designer rats would result in better-defined disease models that can be used in physiologic and applied pharmacologic studies to better treat human essential hypertension. Copyright © 2001 by Current Science Inc.
引用
收藏
页码：12 / 18
页数：6
相关论文
共 26 条
  • [1] Ward R., Familial aggregation and genetic epidemiology of blood pressure, Hypertension: Pathophysiology, Diagnosis and Management, pp. 81-100, (1990)
  • [2] Hamet P., Pausova Z., Adarichev V., Et al., Hypertension: Genes and environment, J Hypertens, 16, pp. 397-418, (1998)
  • [3] Dominiczak A., Negrin D.C., Clark J.S., Et al., Genes and hypertension: From gene mapping in experimental models to vascular gene transfer strategies, Hypertension, 35, pp. 164-172, (2000)
  • [4] Simon D., Karet F.E., Hamdan J.M., Et al., Bartter's syndrome, hypokalaemic alkalosis with hypercalciuria, is caused by mutations in the Na-K-2Cl cotransporter NKCC2, Nature Genet, 13, pp. 183-188, (1996)
  • [5] Simon D., Karet F.E., Rodriguez-Soriano J., Et al., Genetic heterogeneity of Bartter's syndrome revealed by mutations in the K+ channel, ROMK, Nature Genet, 14, pp. 152-156, (1996)
  • [6] Shimkets R.A., Warnock D.G., Bositis C.M., Et al., Liddle's syndrome: Heritable human hypertension caused by mutations in the B subunit of the epithelial sodium channel, Cell, 79, pp. 407-414, (1994)
  • [7] Casari G., Barlassina C., Cusi D., Et al., Association of the alpha-adducin locus with essential hypertension, Hypertension, 25, pp. 320-326, (1995)
  • [8] Jeunemaitre X., Soubrier F., Kotelevtsev Y.V., Et al., Molecular basis of human hypertension: Role of angiotensinogen, Cell, 71, pp. 169-180, (1992)
  • [9] Jeunemaitre X., Lifton R.P., Hunt S.C., Et al., Absence of linkage between the angiotensin converting enzyme locus and human essential hypertension, Nature Genet, 1, pp. 72-75, (1992)
  • [10] Harrap S., Davidson H.R., Conor J.M., Et al., The angiotensin I-converting enzyme gene and predisposition to high blood pressure in man, Hypertension, 21, pp. 455-460, (1993)
123