Ramipril dose-dependently increases nitric oxide availability in the radial artery of essential hypertension patients

Lorenzo Ghiadoni, Daniele Versari, Armando Magagna, Isabella Kardasz, Yvonne Plantinga, Chiara Giannarelli, Stefano Taddei, Antonio Salvetti

Research output: Contribution to journalArticlepeer-review

57 Scopus citations

Abstract

DESIGN AND PARTICIPANTS: A double-blind, crossover, randomized study was designed to evaluate the effect of 3-month treatment with a lower versus a higher antihypertensive dosage of ramipril (5 or 10 mg/day) on nitric oxide (NO)-dependent vasodilation in 46 untreated patients with essential hypertension. Radial artery flow-mediated dilation (FMD), before and after the intra-arterial infusion of N-monomethyl-L-arginine (L-NMMA), to block NO synthase, and the response to sublingual glyceril trinitrate (GTN, 25 μg) were measured at baseline and after the two treatment periods as a change in artery diameter (computerized system from ultrasound scans). Plasma angiotensin II and oxidative stress markers were also assessed. RESULTS: FMD was significantly (P < 0.01) lower in hypertensive patients (4.6 ± 1.8%) than in normotensive subjects (7.1 ± 2.6%), whereas the response to GTN was similar. L-NMMA significantly (P < 0.001) inhibited FMD in normotensive but not in hypertensive subjects. Mean 24-h ambulatory blood pressure, plasma angiotensin II and oxidative stress marker levels were similarly reduced at the end of the two treatment periods. Both dosages of ramipril significantly (P < 0.001) increased FMD (5 mg: 5.9 ± 2.1%; 10 mg: 6.3 ± 2.4%) without modifying the response to GTN. However, compared with baseline (11 ± 19%), the inhibiting effect of L-NMMA on FMD (NO-dependent FMD) was significantly (P < 0.01) greater with ramipril 10 mg (49 ± 12%) than 5 mg per day (38 ± 15%). The improvement in FMD and NO-dependent FMD was not related to changes in plasma levels of angiotensin II or markers of oxidative stress. CONCLUSION: Treatment with ramipril at a higher dosage induced a greater improvement in NO-dependent vasodilation compared with the lower antihypertensive dosage in hypertensive patients.

Original languageEnglish
Pages (from-to)361-366
Number of pages6
JournalJournal of Hypertension
Volume25
Issue number2
DOIs
StatePublished - Feb 2007
Externally publishedYes

Keywords

  • Angiotensin II
  • Angiotensin-converting enzyme inhibitors
  • Endothelium
  • Hypertension
  • Nitric oxide

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