Renal hemodynamic changes induced by captopril and angiotensin-converting enzyme gene polymorphism

Nephron. 1997;75(3):310-4. doi: 10.1159/000189554.

Abstract

We studied the relationship between renal hemodynamic changes induced by a single acute administration of captopril (50 mg p.o.) and angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism in 27 healthy human volunteers, 7 with DD genotype, 10 with ID, and 10 with II genotype. The increase in effective renal plasma flow (p < 0.02) and the fall in renal vascular resistance (p < 0.01) in response to captopril were significantly less in subjects with the DD genotype than in subjects with the other genotypes. These data suggest that intrarenal ACE inhibition by captopril differs according to ACE gene ID polymorphism in healthy humans.

MeSH terms

  • Adult
  • Angiotensin-Converting Enzyme Inhibitors / pharmacology*
  • Blood Flow Velocity / drug effects
  • Blood Pressure / drug effects
  • Captopril / pharmacology*
  • Electrophoresis, Polyacrylamide Gel
  • Female
  • Genotype
  • Hematocrit
  • Humans
  • Male
  • Middle Aged
  • Mutation / genetics
  • Peptidyl-Dipeptidase A / genetics*
  • Polymerase Chain Reaction
  • Polymorphism, Genetic / genetics
  • Renal Circulation / drug effects*
  • Renal Plasma Flow, Effective / drug effects*
  • Vascular Resistance / drug effects*

Substances

  • Angiotensin-Converting Enzyme Inhibitors
  • Captopril
  • Peptidyl-Dipeptidase A