Does Prostaglandin Release Contribute to the Hypotension Induced by Inhibitors of Angiotensin Converting Enzyme?

  • Kevin Mullane
  • Salvador Moncada
  • John R. Vane


The concept that angiotensin converting enzyme inhibitors might be useful therapeutic agents in the treatment of hypertension became a practical proposition in the mid-1960s as a result of the collaborative efforts of workers from quite different fields. In Brazil, Ferreira and co-workers1,2 had shown that metal chelating agents inhibited the inactivation of bradykinin by blood. Some thiol compounds such as BAL also potentiated the actions of bradykinin in vitro and in vivo.1 At that time it was known that the venom of the Brazilian snake Bothrops jararaca induced contraction of the isolated ileum of the guinea pig. While studying this effect, Ferreira et al. noticed that the venom itself strongly potentiated the effects of bradykinin.3 The authors then showed that the venom contained a peptide factor which was responsible for the potentiation and called this “bradykinin potentiating factor” or BPF.4 They also showed that this peptidic extract potentiated both the contractions induced by bradykinin on the guinea pig ileum in vitro and the hypotensive effect of the kinin in the cat and dog in vivo. This potentiation was later correlated with inhibition of kinin-inactivating enzymes.5,6


Angiotensin Converting Enzyme Inhibitor Converting Enzyme Plasma Renin Activity Hypotensive Effect Prostaglandin Release 
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Copyright information

© Plenum Publishing Corporation 1983

Authors and Affiliations

  • Kevin Mullane
    • 1
  • Salvador Moncada
    • 1
  • John R. Vane
    • 1
  1. 1.Wellcome Research LaboratoriesBeckenham, KentEngland

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