The mechanism of the angiotensin-converting enzyme inhibitor quinapril is not related to bradykinin level in heart tissue

Peptides. 2002 Jun;23(6):1161-9. doi: 10.1016/s0196-9781(02)00050-5.

Abstract

In order to examine the effect of the angiotensin-converting enzyme inhibitor (ACEi) quinapril, we performed a sensitive and specific radioimmunoassay (RIA) to quantify bradykinin, BK-(1-9), in heart and kidney tissues. The BK-(1-9) level was unaffected in the heart of sham and water-deprived rats treated for 2h with quinapril (10mg/kg), but was significantly higher in the kidneys in the two groups. In these conditions, circulating and tissue angiotensin II (Ang II) levels were significantly decreased by quinapril. Moreover, our results indicated that acute treatment with this dose of quinapril induced kinin-mediated effects which were not related to its action on bradykinin degradation in rat hearts.

MeSH terms

  • Angiotensin I / biosynthesis
  • Angiotensin I / blood
  • Angiotensin II / biosynthesis
  • Angiotensin II / blood
  • Angiotensin-Converting Enzyme Inhibitors / pharmacology*
  • Animals
  • Bradykinin / biosynthesis*
  • Isoquinolines / pharmacology*
  • Kidney / metabolism
  • Male
  • Myocardium / metabolism*
  • Peptidyl-Dipeptidase A / metabolism
  • Quinapril
  • Radioimmunoassay
  • Rats
  • Rats, Wistar
  • Reproducibility of Results
  • Sensitivity and Specificity
  • Tetrahydroisoquinolines*
  • Time Factors
  • Tissue Distribution

Substances

  • Angiotensin-Converting Enzyme Inhibitors
  • Isoquinolines
  • Tetrahydroisoquinolines
  • Angiotensin II
  • Angiotensin I
  • Peptidyl-Dipeptidase A
  • Quinapril
  • Bradykinin