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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Mechanism and modification of bradykinin-induced coronary vasodilation.

In isolated perfused rabbit hearts, bradykinin produced a concentration-dependent decrease in coronary resistance directly associated with biosynthesis and release of prostaglandin-E-like substance. An inhibitor of bradykinin destruction (the nonapeptide SQ-20881) markedly enhanced both the coronary vasodilation and release of prostaglandin-E-like substance produced by cardiac injection of bradykinin. Indomethacin inhibited both the myocardial prostaglandin biosynthesis and the decrease in coronary resistance induced by bradykinin. The demonstration that bradykinin is a potent stimulator of prostaglandin biosynthesis in the heart has implications as to the cause of the afferent cardiovascular reflexes and pain in myocardial infarction and angina pectoris.[1]

References

  1. Mechanism and modification of bradykinin-induced coronary vasodilation. Needleman, P., Key, S.L., Denny, S.E., Isakson, P.C., Marshall GROUSI, Missouri 63110, n.u.l.l. Proc. Natl. Acad. Sci. U.S.A. (1975) [Pubmed]
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