Why the study?
Does local intra-arterial infusion of enalaprilat augment endothelium-dependent vasodilation in healthy volunteers?
Does local intra-arterial infusion of enalaprilat augment endothelium-dependent vasodilation in healthy volunteers?
ACE inhibitors augment endothelium-dependent vasodilation in healthy human vasculature, likely by potentiating nonprostanoid endothelium-derived relaxing factor.
Supports ACE inhibitor effects on endothelial function in healthy vessels; hypothesis-generating and should not yet change practice.
We have examined the effects of local intra-arterial infusion of enalaprilat (an angiotensin converting enzyme inhibitor) on responses initiated by concomitantly infused acetylcholine (an endothelium-dependent vasodilator) and sodium nitroprusside (a direct dilator of smooth muscle) in the forearm arterial beds of healthy volunteers. Although the angiotensin converting enzyme inhibitor alone did not affect basal forearm blood flow or vascular resistance, it significantly augmented the increase in blood flow and reduction in vascular resistance induced by acetylcholine (both p < 0.05). Coinfusion of enalaprilat did not enhance sodium nitroprusside-induced vasodilation. Pretreatment with NG-monomethyl-L-arginine blocked the augmentation of blood flow induced by the angiotensin converting enzyme inhibitor. The effect of enalaprilat was still observed after the administration of acetylsalicylic acid (p < 0.05). These results suggest that angiotensin converting enzyme inhibitors potentiate nonprostanoid endothelium-derived relaxing factor in normal human forearm vasculature.
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Nakamura et al. (1992) studied this question.
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