Improvement of bradykinin endothelium-mediated vasodilation of forearm resistance circulation by quinaprilat in patients with coronary artery diseasewith or without left ventricular dysfunction

Angiotensin-converting enzyme (ACE) inhibition potentiates bradykinin and a cetylcholine endothelium-mediated vasodilation. Three groups were studied. Group I (n = 10) was the reference group; group II was composed of nine pat ients with coronary artery disease; and group III of seven patients with co ronary artery disease and left ventricular dysfunction. Forearm blood flow was measured with plethysmography. Acetylcholine and bradykinin were admini stered in a random order in the brachial artery at infusion rates of 40 and 80 mu g/min and 10, 30, 100 pmol/min, respectively. Then quinaprilat was i nfused alone at the rate of 50 mu g/min and then coinfused with acetylcholi ne and bradykinin. Five of the reference subjects were pretreated with acet ylsalicylate. Acetylcholine and bradykinin increased forearm blood now in a dose-dependent manner in the three groups. However, the vasodilator respon ses to both agents were significantly lower in the two groups of patients t han in the reference group. Quinaprilat significantly enhanced the vasodila tor response to acetylcholine only in subjects of the reference group, wher eas it enhanced the vasodilator response to each dose of bradykinin, both i n subjects of the reference group and in patients. Pretreatment with aspiri n did not change the vasodilator responses in any group, In healthy persons , quinaprilat had no effect on its own on forearm blood flow but enhanced t he response to bradykinin and even acetylcholine. In patients with coronary disease, short-term administration of quinaprilat was able to improve the impaired response to bradykinin. The response to acetylcholine, however, co uld not be significantly enhanced in contrast to that in healthy subjects.