Many studies reported that endothelium-dependent vasodilator response is impaired in patients with congestive heart failure. But the opposite results also were reported. The aim of this study was to determine the presence of endothelial dysfunction and its characteristics.

Forearm blood flow was measured in 12 patients with congestvie heart failure (7 males and 5 females, mean age 53±11 years old) and 10 normal control subjects (5 males and 5 females, mean age 41±10 years old) using strain-gauge plethysmography. The endothelium-dependent vasodilators were acetylcholine (7.5, 15, and 30 microgram/min), which uses a pertussis toxin-sensitive signal transduction pathway, and bradykinin (100, 200, and 400 ng/min), which uses a pertussis toxin-insensitive signal transduction pathway to activate nitric oxide production. Sodium nitroprusside (0.8, 1.6, and 3.2 microgram/min) was used as an endothelium-independent vasodilator. All drugs were infused into the brachial artery with random order.

The basal forearm blood flow was similar between both groups. The maximum flow in response to acetylcholine, bradykinin, and sodium nitroprusside was also similar in two groups.

Patients with congestive heart failure showed normal endothelium-dependent vasodilator responses to both acetylcholine and to bradykinin. This finding indicates that the endothelial vasodilator function is normal in the patients with heart failure.