Sulfhydryl angiotensin-converting enzyme inhibition induces sustained reduction of systemic oxidative stress and improves the nitric oxide pathway in patients with essential hypertension

Am Heart J. 2004 Jul;148(1):e5. doi: 10.1016/j.ahj.2004.03.025.

Abstract

Background: Essential hypertension is associated with enhanced LDL oxidation and impaired endothelium-dependent vasodilation. The antioxidant status is linked to the nitric oxide (NO) pathway. Sulfhydryl angiotensin-converting enzyme (ACE) inhibitors inhibit oxidative stress and atherogenesis in experimental models; therefore we tested whether this beneficial antioxidant activity could be also clinically relevant in patients with essential hypertension.

Methods: Plasma LDL oxidizability was investigated initially in untreated normocholesterolemic patients with moderate essential hypertension without clinically evident target organ damage (n = 96) and in control normotensive subjects (n = 46). Patients were then randomly assigned into two age- and sex-matched groups to receive the new sulfhydryl ACE inhibitor zofenopril (15 to 30 mg/d; n = 48) or enalapril (20 mg/d, n = 48). LDL oxidizability was evaluated (generation of malondialdehyde, MDA) and systemic oxidative stress was evaluated by isoprostanes (8-isoPGF2alpha). Asymmetrical dimethyl-L-arginine (ADMA), a competitive inhibitor of endothelial NO synthase, and plasma nitrite and nitrates (NOx) were also measured.

Results: LDL from hypertensive subjects had enhanced susceptibility to oxidation in vitro compared with that in control subjects (P <.05). Similarly, isoprostanes were significantly increased (P <.01) in hypertensive subjects versus control subjects. After 12-week treatment, MDA levels were significantly reduced by zofenopril (P <.05) but not enalapril treatment (P = not significant). Isoprostanes were normalized after zofenopril treatment (P <.03), whereas enalapril was ineffective. After treatment with both ACE inhibitors, plasma NOx concentrations were significantly reduced (P <.05). Similarly, hypertension increased ADMA concentration compared with the normotensive state, whereas ACE inihibition elicited a significant decrease. However, the reduction of ADMA concentration was significantly higher in patients receiving sulfhydryl ACE inhibition (P <.05 vs enalapril).

Conclusions: The sulfhydryl ACE inhibitor zofenopril reduces oxidative stress and improves the NO pathway in patients with essential hypertension. If confirmed in a large multicenter clinical trial, our data suggest a possible vasculoprotective effect of the compound in retarding vascular dysfunction and atherogenesis that often develops rapidly in hypertensive patients.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial

MeSH terms

  • Angiotensin-Converting Enzyme Inhibitors / pharmacology*
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use
  • Arginine / analogs & derivatives*
  • Arginine / metabolism
  • Captopril / analogs & derivatives*
  • Captopril / pharmacology*
  • Captopril / therapeutic use
  • Enalapril / pharmacology*
  • Enalapril / therapeutic use
  • Female
  • Humans
  • Hypertension / drug therapy*
  • Hypertension / metabolism
  • Lipid Peroxidation / drug effects
  • Lipoproteins, LDL / metabolism
  • Male
  • Middle Aged
  • Nitrates / blood
  • Nitric Oxide / metabolism*
  • Nitrites / blood
  • Oxidative Stress / drug effects*

Substances

  • Angiotensin-Converting Enzyme Inhibitors
  • Lipoproteins, LDL
  • Nitrates
  • Nitrites
  • zofenopril
  • Nitric Oxide
  • N,N-dimethylarginine
  • Enalapril
  • Arginine
  • Captopril