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Targeting flight-or-fight hormone response to combat heart failure
Date:6/24/2010

disease strain-related thickening of muscle tissue (hypertrophy) and scar tissue formation (fibrosis). Both compounds partially normalized the force of heart muscle contraction by making sure the beta adrenergic receptors became and remained responsive to adrenalin. This was done by both decreasing overall levels of GRK2 in the heart and by limiting its effectiveness.

M119 and Gallein have been used in a similar way in the past to target the receptor desensitization process that occurs in other conditions, such as chronic pain. For example, Smrcka and his collaborator Jean Bidlack, Ph.D., professor of Pharmacology and Physiology at the Medical Center, have shown M119 can reverse the desensitization of opiate receptors, which in turn increases the efficacy of painkillers such as morphine. M119 and Gallein are not known drugs; they are compounds that act as dyes, or stains, and were previously not known to have any therapeutic activity.

This research addresses a health problem that affects nearly 6 million Americans. The result of underlying problems like coronary artery disease, high blood pressure or heart attack damage, heart failure is the gradual loss of the heart's ability to pump with enough force to meet the body's need for blood. Half of patients will not live five years past the day they are diagnosed. The best treatment for a severe heart failure patient is a transplant, but with just over 2,000 transplants done each year and more than 3,000 people on the waiting list at any given time, research like this is needed to find new options for patients.


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Contact: Emily Butler
emily_butler@urmc.rochester.edu
585-273-1757
University of Rochester Medical Center
Source:Eurekalert

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