Rosiglitazone Causes Endothelial Dysfunction in Humans
Journal of Cardiovascular Pharmacology and Therapeutics,  Clinical Article

Perampaladas K et al. – Unexpectedly, therapy with rosiglitazone caused abnormalities in endothelial function in normal volunteers. These findings have important implications with respect to drug development and surveillance.

  • In this double–blind, randomized, placebo–controlled study, 44 participants were randomized to placebo, rosiglitazone (4 mg twice daily), transdermal GTN (0.6 mg/h), or both GTN and rosiglitazone.
  • After 7 days of treatment, participants underwent measures of forearm blood flow during brachial artery infusion of acetylcholine (Ach).
  • Serum glucose concentrations and insulin sensitivity were assessed.

  • Unexpectedly, rosiglitazone–treated participants experienced blunted responses to endothelium–dependent responses to Ach (P < .05 vs placebo).
  • Sustained GTN administration caused similar abnormalities in endothelial function (P < .05 vs placebo) and rosiglitazone + GTN (P < .05 vs placebo; P = ns vs rosiglitazone).
  • Interestingly, co–infusion of the antioxidant vitamin C improved endothelial responses in those randomized to rosiglitazone and GTN alone (P = not significant [ns] compared with placebo), but it did not improve endothelial function in those treated with rosiglitazone + GTN.
  • Neither rosiglitazone nor GTN treatment modified the measures of glucose metabolism.

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