It is believed that aspirin counteracts some of the beneficial action of ACE inhibitors, although the mechanism involved are unknown. It has been speculated that bradykinin or substance P, both potenciated by ACE inhibitors, may be involved.
We have shown that exogenous bradykinin and substance P cause vasodilation in patients with heart failure, that there is no effect of intra arterial on its own, and thede is no effect or aspirin, intra arterial or oral, on the responses to bradykinin and substance P. Demonstrasion of these responsive to bradykinin and substance is novel in patients with heart failure, and is only partly consistent with previous wodk in vitro, in animals and in healty vollunterss.
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