JCI Table of Contents, Apr...( echanism called the renin-angiotensin s...),Health

echanism called the renin-angiotensin system (RAS), in which the protein angiotensinogen is sequentially cleaved by renin (then by another enzyme called ACE) to form the biologically active peptide, angiotensin II (AngII). The secretion of renin is tightly linked to salt intake and the pressure inside the kidney, suggesting that the RAS is central to controlling body fluid volume and blood pressure. Now, in a study appearing in the April issue of the Journal of Clinical Investigation, researcher Roberto Levi and colleagues at Weill Medical College of Cornell University, New York report that cells called mast cells, known to be involved in asthma and allergy, also produce renin. The authors studied isolated guinea pig hearts and found that cardiac mast cells can release renin, and that this release results in the formation of angiotensin in sufficient amounts to cause disease-associated events such as release of norepinephrine (a stress hormone involved in the "fight or flight" response) and cardiac arrythmias (irregular heartbeat). The researchers confirmed that the angiotensin was formed through the action of renin by treating the hearts with an inhibitor of renin, which abolished angiotenisn formation. The researchers confirmed these results using hearts obtained from mice. Production of renin by cardiac mast cells represents a novel mechanism for regulating RAS. The authors note that these findings imply that mast cell-derived renin may be a useful therapeutic target for cardiac dysfunctions associated with arrhythmias, cardiac death, heart attack, and heart failure.

In an accompanying commentary, Thomas M. Coffman from the Durham VA Medical Center in North Carolina states that "although the precise basis for control of renin in mast cells is not clear, this will be a critical area for future research. This discovery suggests a distinct pathway for activation of the RAS that may have a particular impact in the pathogenesis of chronic tissue injury as
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Contact: Brooke Grindlinger
press_releases@the-jci.org
212-342-9006
Journal of Clinical Investigation
3-Apr-2006

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