期刊
ATHEROSCLEROSIS
卷 148, 期 1, 页码 43-47出版社
ELSEVIER SCI IRELAND LTD
DOI: 10.1016/S0021-9150(99)00220-8
关键词
atherosclerosis; von Willebrand factor; nitric oxide; desmopressin
Increased release of von Willebrand factor (vWF) has been linked to the pathogenesis of atherosclerosis. For this complex disease, impairment of endothelium-derived, nitric oxide production and impaired vascular relaxation has also been reported. Since endothelially produced nitric oxide (NO) is known to inhibit secretion of the Weibel-Palade bodies in animals, we hypothesized that NO could mitigate VWF secretion. Tn a randomized, placebo controlled cross-over trial, eight male volunteers received N-monomethyl-L-arginine (LNMMA) to block endothelial NO production or placebo, and VWF release was stimulated by infusing desmopressin in three cumulative doses (0.05, 0.15, 0.4 mu g/kg) in both periods. At a threshold dose of 0.15 mu g/kg desmopressin, concomitant partial blockade of NO production resulted in 20% higher levels of VWF (P<0.04). However, maximal VWF release after 0.4 mu g/kg desmopressin was unaffected by L-NMMA (Delta 7% between periods, P = 0.88). These data show the dampening effect of NO production on VWF release in response to threshold concentrations of secretagogues. This may in part explain the higher vWF levels in cardiovascular diseases associated with impaired endothelial NO generation. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据