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ShareScienceDaily (Jan. 5, 2009) — Individuals who have persistent high blood pressure are at increased risks of a number of serious medical conditions, including heart failure. One of the factors that contributes to such heart failure is thickening of the muscle wall of the heart.
Such thickening (known as hypertrophy) is a compensatory response of the heart to the high blood pressure.
A team of researchers at Johns Hopkins University, Baltimore, has provided new insight into both the signaling mechanisms by which high blood pressure leads to compensatory hypertrophy of the mouse heart and the molecular mechanisms by which a heart failure drug in clinical trials works.
In the study, which was led by Eiki Takimoto and David Kass, when mice lacking the protein RGS2 were manipulated such that they had persistent high blood pressure they developed hypertrophy of the muscle wall of the heart more rapidly than normal mice manipulated in the same way.
Further, these mice went on to exhibit heart failure and died at a young age. Additional analysis indicated that a drug that prevents hypertrophy by targeting the protein PDE5 was less effective at preventing hypertrophy caused by high blood pressure in RGS2-deficient mice than in normal mice.
These data have clinical implications, as they provide insight into the mechanism by which PDE5 inhibitors, which have recently entered clinical trials to treat a form of heart failure, work.
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The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Regulator of G protein signaling 2 mediates cardiac compensation to pressure overload and antihypertrophic effects of PDE5 inhibition in mice. Journal of Clinical Investigation, Jan 6, 2009
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
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