Cardiac hypertrophy, or thickening of the heart muscle, occurs naturally in athletes but may also be a pathological response to high blood pressure or stenosis of the aortic valve. Pathological hypertrophy allows the heart to continue pumping blood against the increased pressure but, over time, can lead to loss of function and heart failure. Researchers at the University of California, Davis, have now identified soluble epoxide hydrolase (sEH) as a key enzyme in the development of angiotensin II (Ang II)-mediated cardiac hypertrophy. sEH hydrolyses the blood pressure-regulating epoxyeicosatrienoic acids (EETs) into dihydroxyeicosatrienoic acids (DHETs), which show reduced biological activity. The study, which is published in the January 13th issue of the Proceedings of the National Academy of Sciences showed that levels of sEH in the heart were elevated in two rodent models of Ang II-induced hypertrophy. The Ang II receptor blocker, losartan, prevented the increase in sEH and administration of an inhibitor of sEH, 1-(1-acetyl-piperidin-4-yl)-3-(4-trifluoromethoxy-phenyl)-urea (TUPS), prevented the pathogenesis of Ang II-induced hypertrophy.
The authors suggest that inhibition of sEH could be a useful approach to treat Ang II-induced cardiac hypertrophy. Existing treatments for heart failure include β-blockers, angiotensin converting enzyme (ACE) inhibitors or Ang II receptor blockers, diuretics and drugs that improve the heart’s ability to pump.
In another study, published in the journal Clinical Science, administration of a different sEH inhibitor, 12-(3-adamantan-1-yl-ureido)-dodecanoic acid (AUDA), was found to reduce kidney damage caused by Ang II-induced hypertension in spontaneously diabetic rats.
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