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Although normally clinically silent, persistent hypertension and atherosclerosis are leading risk factors for strokes, heart attacks, heart failure, aneurysms and chronic renal failure. How blood pressure is regulated is still not fully understood, but a team lead by scientists at the University of Pennsylvania School of Medicine has now suggested a role for prostaglandin F2α (PGF2α) in increasing blood pressure and accelerating atherosclerosis. Prostaglandins are a group of hormone-like substances that mediate many physiological and pathophysiological processes, and the team found that mice lacking the receptor for PGF2α had lower blood pressure and less atherosclerosis than wild-type mice. Knocking out the PGF2α receptor was found to suppress activity of the renin-angiotensin system which plays a key role in regulating blood pressure. When blood pressure is low, the liver secretes a protein, angiotensinogen, which is cleaved by renin to give angiotensin I. Further cleavage by angiotensin converting enzyme (ACE) produces angiotensin II which increases blood pressure by narrowing blood vessels and by stimulating release of aldosterone which leads in turn to retention of sodium and water.

If the results seen in mice translate to humans, blocking the PGF2α receptor may provide a novel strategy for controlling blood pressure and reducing atherosclerosis. The study is published in full in the Proceedings of the National Academy of Sciences.

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