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Human Molecular Genetics Advance Access published online on November 8, 2005
Human Molecular Genetics, doi:10.1093/hmg/ddi412
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© The Author 2005. Published by Oxford University Press. All rights reserved

Article

A loss of genome buffering capacity of Dahl salt sensitive model to modulate blood pressure as a cause of hypertension

Sophie Charron 1, Raphaëlle Lambert 1, Vasiliki Eliopoulos 1, Chenda Duong 1, Annie Ménard 1, Julie Roy 1, and Alan Y. Deng 2*

1 Research Centre-CHUM, Montréal, Québec, H2W 1T8, Canada
2 Research Centre, Centre Hospitalier de l'Université de Montréal (CHUM), 7-132 Pavillon Jeanne Mance, 3840, rue St. Urbain, Montreal, Quebec, H2W 1T8, Canada

* To whom correspondence should be addressed.
Alan Y. Deng, E-mail: alan.deng{at}umontreal.ca


  Abstract

Essential hypertension is a complex trait influenced by multiple genes known as quantitative trait loci (QTLs) for blood pressure (BP). It is not clear, however, what roles these QTLs play in maintaining normotension. Insights gained toward the maintenance of normotension will shed light on how hypertension can result from a deficiency or malfunctioning of this maintenance. Currently, congenic strains were systematically constructed using Dahl salt sensitive (DSS) and Lewis rats not only to define QTLs (i.e. in DSS background), but also to ascertain effects of the same QTLs in preserving normotension (i.e. in Lewis background), a first such study. Results showed that although Lewis alleles for two QTLs on Chromosome (Chr) 18 lowered BP on the DSS background, their BP-increasing DSS alleles failed to influence BP in the Lewis background. To further prove that the Lewis background is resistant and the DSS background is susceptible to the effects of QTLs, BP-increasing alleles of a QTL on Chr 2 were introgressed into the DSS background, and its BP-decreasing alleles into the Lewis background. Indeed, there was no BP-decreasing effect on the Lewis background while demonstrating a BP-increasing effect on the DSS background. Thus, a genetic regulation of BP QTLs in the Lewis genome inhibits BP changes by nullifying the effects of BP-altering QTLs. In comparison, the DSS genome must have lost the buffering capacity for stabilizing BP. The current work presents good evidence that a lack of regulation for functions of BP QTLs is a potential underlying cause of hypertension.


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