Send to

Choose Destination
See comment in PubMed Commons below
Curr Hypertens Rep. 2011 Feb;13(1):21-8. doi: 10.1007/s11906-010-0173-8.

Epigenetics and hypertension.

Author information

Department of Physiology & Biophysics, Howard University College of Medicine, 520 "W" Street NW, Washington, DC 20059, USA.


Epigenetics refers to mechanisms for environment-gene interactions (mainly by methylation of DNA and modification of histones) that do not alter the underlying base sequence of the gene. This article reviews evidence for epigenetic contributions to hypertension. For example, DNA methylation at CpG islands and histone acetylation pathways are known to limit nephron development, thereby unmasking hypertension associated with exposure to a high-salt diet. Maternal water deprivation and protein deficiency are shown to increase expression of renin-angiotensin system genes in the offspring. The methylation pattern of a serine protease inhibitor gene in human placentas is shown to be a marker for preeclampsia-associated hypertension. Mental stress induces phenylethanolamine n-methyltransferase, which may act as a DNA methylase and mimic the gene-silencing effects of methyl CpG binding protein-2 on the norepinephrine transporter gene, which, in turn, may exaggerate autonomic responsiveness. A disrupter of telomeric silencing (Dot1) is known to modulate the expression of a connective-tissue growth-factor gene associated with blood vessel remodeling, which could alter vascular compliance and elastance. Dot1a also interacts with the Af9 gene to produce high sodium channel permeability and silences the hydroxysteroid dehydrogenase-11β2 gene, thereby preventing metabolism of cortisol to cortisone and overstimulating aldosterone receptors. These findings indicate targets for environment-gene interactions in various hypertensive states and in essential hypertension.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center