Journal
HYPERTENSION RESEARCH
Volume 32, Issue 5, Pages 347-357Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/hr.2009.27
Keywords
antihypertensive agents; cardiac hypertrophy; gene expression profiling
Categories
Funding
- Health Research Board
- European Union
- Irish Programme for Research in Third Level Institutions
- Spanish Cardiovascular network [RD06/0014/0035]
- Comunidad Autonoma de Madrid [S-GEN-0247/2006]
- SAF [2007/63648, P-BIO-0194-2006]
- Spanish Ministry of Science and Innovation.
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Left ventricular hypertrophy (LVH), a common consequence of systemic hypertension associated with poor clinical outcome, is also a potentially reversible condition. Here, we probed the molecular pathways that underpin the development of LVH and their modulation by antihypertensive regimens that reversed LVH. Spontaneously hypertensive rats were studied at 12 (early LVH) and 48 weeks ( late LVH), respectively, with normotensive Wistar-Kyoto rats as age-matched controls. Three treatment groups were maintained for 36 weeks on the following regimens: (1) quinapril, (2) doxazosin and quinapril combination, and (3) losartan. Gene expression profiling was performed with Affymetrix microarrays (GeneChip Rat-230A) and primary function-focused average linkage hierarchical cluster analysis. Of the 15 696 gene sequences expressed on the Affymetrix GeneChip Rat-230A, there was significant alteration in the expression of 295 (1.9%) of these transcripts in 'early' LVH and 143 (0.9%) in 'late' LVH. The predominant changes in gene expression were seen in metabolism, cell growth/proliferation, signal transduction, development and muscle contraction/cytoskeleton functional groups. Although sharing many effects on gene expression, the three treatments showed different expression profiles. Despite significant regression of LVH with treatment, 31 LVH-associated transcripts were unchanged by any of the treatment groups. Our data suggest that LVH regression does not normalize the LVH transcriptome. Therefore, regression of hypertension-induced LVH is associated with a distinct gene expression profile, suggesting the effect of both treatment and a previously unknown specific myocardial physiology after regression of LVH. Hypertension Research (2009) 32, 347-357; doi:10.1038/hr.2009.27; published online 27 March 2009
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