Human studies evaluating the effects of DM on endothelium-dependent vasodilation have yielded some conflicting results, although they generally corroborate those found in animal studies. Saenz de Tejada et al. (60) studied penile tissue excised from men with erectile dysfunction and found that endothelium-dependent relaxation is reduced in the corpus cavernosa of impotent men with diabetes relative to those who are nondiabetic.
However, in vivo studies involving human subjects with insulin-dependent diabetes have demonstrated both blunted and normal vasodilatory responses to acetylcholine, methacholine, or carbachol (the latter two being acetylcholine analogs) in forearm resistance vessels in patients with DM (61-63). To evaluate in vivo endothelial function in these vessels, we and others have employed the venous occlusive plethysmography technique. Type 1 diabetic (61) individuals were shown to have impaired endothelium-dependent responses to methacholine in the forearm resistance vessels (Fig. 2A). The vasodilator response to both nitroprusside (Fig. 2B) and verapamil, both endothelium-independent, were preserved. In this study, all the patients were taking aspirin, making it unlikely that vasodilator prostanoids were responsible for the altered endothelium-dependent relaxation. The degree of attenuation of forearm blood flow (FBF) response
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