Schulz R, Triggle C R
Department of Paediatrics, Faculty of Medicine, University of Alberta, Edmonton, Canada.
Trends Pharmacol Sci. 1994 Jul;15(7):255-9. doi: 10.1016/0165-6147(94)90321-2.
NO is a key transducer of a vasodilator message from the endothelium to vascular smooth muscle. Recently, its actions as a negative inotrope in cardiac muscle have been discovered. In the vasculature, it is synthesized under physiological conditions following activation of a low-output, Ca(2+)-dependent NO synthase (NOS) in endothelial cells. Immune activation triggers the expression of a high-output, Ca(2+)-independent NOS in the vasculature and myocardium, causing the overproduction of NO and significant cardiovascular dysfunction. In this article, Richard Schultz and Chris Triggle briefly review recent findings concerning the role of NO, and other endothelium-derived factors, in vascular smooth muscle function and consider the consequences of its production in the heart.
一氧化氮（NO）是血管舒张信号从内皮传递至血管平滑肌的关键转导分子。最近，人们发现它在心肌中具有负性肌力作用。在血管系统中，生理条件下内皮细胞中低产量、钙（Ca2+）依赖的一氧化氮合酶（NOS）激活后会合成一氧化氮。免疫激活会触发血管系统和心肌中高产量、钙（Ca2+）非依赖的一氧化氮合酶的表达，导致一氧化氮过度产生及严重的心血管功能障碍。在本文中，理查德·舒尔茨和克里斯·特里格尔简要回顾了关于一氧化氮及其他内皮衍生因子在血管平滑肌功能中的作用的近期研究发现，并探讨了其在心脏中产生的后果。
