Vanhoutte Paul M
State Key Laboratory of Pharmaceutical Biotechnology and Department of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, HKSAR, China.
Ann Vasc Dis. 2018 Mar 25;11(1):41-51. doi: 10.3400/avd.ra.17-00134.
This essay summarizes a lecture presented on October 19th, 2017, during the 58th Annual Meeting of the Japanese College of Angiology in Nagoya, Japan. The lecture summarizes several instances where the absence of relaxations of isolated blood vessels in response to endothelium-dependent vasodilator agonists, which cause activation of endothelial nitric oxide synthase (eNOS) and consequent production of endothelium-derived nitric oxide (NO) and stimulation of soluble guanylyl cyclase (sGC) in underlying vascular smooth muscle, or hypoxia are curtailed or reversed to endothelium-dependent contractions. Chosen examples include selective dysfunction of eNOS activation in regenerated endothelial cells, unresponsiveness of vascular smooth muscle cells to NO during subarachnoid hemorrhage, and biased activation of sGC in vascular smooth muscle cells during acute exposure to hypoxia. The main message of this essay is that absence, blunting, or reversal of endothelium-dependent relaxations in response to vasodilator agonists cannot necessarily be interpreted as a sign of endothelial dysfunction. (This is a review article based on the invited lecture of the 58th Annual Meeting of Japanese College of Angiology.).
本文总结了2017年10月19日在日本名古屋举行的第58届日本血管外科学会年会上发表的一次演讲。该演讲总结了几个实例，即孤立血管对内皮依赖性血管舒张激动剂无松弛反应（这些激动剂会激活内皮型一氧化氮合酶（eNOS），进而产生内皮源性一氧化氮（NO），并刺激下层血管平滑肌中的可溶性鸟苷酸环化酶（sGC））或缺氧的情况被减少或转变为内皮依赖性收缩。所选实例包括再生内皮细胞中eNOS激活的选择性功能障碍、蛛网膜下腔出血期间血管平滑肌细胞对NO无反应，以及急性缺氧期间血管平滑肌细胞中sGC的偏向性激活。本文的主要观点是，对血管舒张激动剂的内皮依赖性舒张反应缺失、减弱或逆转不一定能被解释为内皮功能障碍的迹象。（这是一篇基于第58届日本血管外科学会年会特邀演讲的综述文章。）
