Mice lacking this key protein had reduced cardiac tolerance for both exercise- and adrenaline-like stress. Nearly three-quarters (73 percent) of the Kir6.2-deficient mice died within 14 minutes after a stressor challenged their cardiac response -- yet all the mice that possessed Kir6.2 survived the stress tests.
As reported in the Oct. 1 edition of Proceedings of the National Academy of Sciences, the research provides provocative leads to understanding and treating stress-related disorders of the heart. These may range from sudden death of highly conditioned athletes to the cumulative effects of psychological stress at work, school or in family life.
"We have identified in the heart a protective mechanism against stress that is roughly analogous to an automatic sprinkler system that douses a fire in an emergency," says Andre Terzic, M.D., Ph.D, lead researcher. "The Kir6.2 protein senses stress and prevents damage to the heart by helping the cells maintain equilibrium even under peak workloads. Lack of Kir6.2 protein function causes sudden, irreversible damage to heart cells, which could lead to heart failure."
In the study, the Mayo Clinic team led by Dr. Terzic compared mice in which the gene that produces the Kir6.2 protein had been eliminated to a control group of mice that possessed the Kir6.2 protein. Their goal was to determine whether Kir6.2 enables heart cells to maintain high levels of activity without suffering damage, and to discover how it works.
Study Findings
In treadmill testing, the normal mice tolerated more than three times the workload that the Kir6.2-deficient mice could. Both groups of mice were also tested under stress induced by a compound similar in effect to adrenaline,
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Contact: Lee Aase
newsbureau@mayo.edu
507-284-5005
Mayo Clinic
27-Sep-2002