SAN DIEGO Heart failure is the most common cause of death throughout the world, typically the result of chronic high blood pressure, also known as hypertension. As a result, research efforts have focused on an array of approaches aimed at preventing and treating high blood pressure. Recently, Japanese researchers examined the utility of an anti-hypertensive drug, moxonidine, which acts on the imidazoline receptors in the cardiovascular center of the brainstem. They found, using an animal model, that the drug can improve heart function and survival independent of its effect on blood pressure. They also found the drug had a favorable effect on oxidative stress, which is related to insulin resistance, the underlying abnormality in diabetes, which is common in people with heart failure.
An abstract presentation about the findings will be offered at the meeting Experimental Biology 2012, being held April 21-25 at the San Diego Convention Center. The study was conducted by Yoshitaka Hirooka, Nobuhiro Honda, Ryuichi Matsukawa, Koji Itou and Kenji Sunagawa, all of the Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences in Fukuoka, Japan. It is entitled, "Central sympathoinibition improves left ventricular function during the transition from hypertrophy to heart failure in Dahl salt-sensitive rats." The abstract is sponsored by the American Society for Investigative Pathology (ASIP), one of six scientific societies sponsoring the conference which last year attracted some 14,000 attendees.
Heart failure is a chronic disease that takes many forms and a variety of medications are used to treat it. Drugs such as ACE inhibitors and beta blockers target the causes of systolic heart failure. Clonidine, a first-generation central sympathoinhibitory drug, targets brain receptors that reduce cardiac output and lower blood pressure. Moxonidine, a second-generation drug, targets diastolic heart failure and function by reduc
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Federation of American Societies for Experimental Biology