|
|
||||||||
Molecular Physiology Laboratory, Centre for Cardiovascular Science, Queens Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom
In this review, we outline the application and contribution of transgenic technology to establishing the genetic basis of blood pressure regulation and its dysfunction. Apart from a small number of examples where high blood pressure is the result of single gene mutation, essential hypertension is the sum of interactions between multiple environmental and genetic factors. Candidate genes can be identified by a variety of means including linkage analysis, quantitative trait locus analysis, association studies, and genome-wide scans. To test the validity of candidate genes, it is valuable to model hypertension in laboratory animals. Animal models generated through selective breeding strategies are often complex, and the underlying mechanism of hypertension is not clear. A complementary strategy has been the use of transgenic technology. Here one gene can be selectively, tissue specifically, or developmentally overexpressed, knocked down, or knocked out. Although resulting phenotypes may still be complicated, the underlying genetic perturbation is a starting point for identifying interactions that lead to hypertension. We recognize that the development and maintenance of hypertension may involve many systems including the vascular, cardiac, and central nervous systems. However, given the central role of the kidney in normal and abnormal blood pressure regulation, we intend to limit our review to models with a broadly renal perspective.
This article has been cited by other articles:
![]() |
M. A. Bailey, J. M. Paterson, P. W.F. Hadoke, N. Wrobel, C. O.C. Bellamy, D. G. Brownstein, J. R. Seckl, and J. J. Mullins A Switch in the Mechanism of Hypertension in the Syndrome of Apparent Mineralocorticoid Excess J. Am. Soc. Nephrol., January 1, 2008; 19(1): 47 - 58. [Full Text] [PDF] |
||||
![]() |
H. Oberleithner, C. Riethmuller, H. Schillers, G. A. MacGregor, H. E. de Wardener, and M. Hausberg Plasma sodium stiffens vascular endothelium and reduces nitric oxide release PNAS, October 9, 2007; 104(41): 16281 - 16286. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. J. Pinho, M. P. Serrao, and P. Soares-da-Silva High-salt intake and the renal expression of amino acid transporters in spontaneously hypertensive rats Am J Physiol Renal Physiol, May 1, 2007; 292(5): F1452 - F1463. [Abstract] [Full Text] [PDF] |
||||
![]() |
Z. Yang, K. Venardos, E. Jones, B. J. Morris, J. Chin-Dusting, and D. M. Kaye Identification of a Novel Polymorphism in the 3'UTR of the L-Arginine Transporter Gene SLC7A1: Contribution to Hypertension and Endothelial Dysfunction Circulation, March 13, 2007; 115(10): 1269 - 1274. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. P. Provoost Does Angiotensin Receptor Recycling Regulate Blood Pressure? Hypertension, September 1, 2006; 48(3): 370 - 371. [Full Text] [PDF] |
||||
![]() |
R. Inoue, L. J. Jensen, J. Shi, H. Morita, M. Nishida, A. Honda, and Y. Ito Transient receptor potential channels in cardiovascular function and disease. Circ. Res., July 21, 2006; 99(2): 119 - 131. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |