Vanhoutte P M
I.R.I.S., Courbevoie, France.
J Mol Cell Cardiol. 1996 Nov;28(11):2233-40. doi: 10.1006/jmcc.1996.0215.
The endothelium is a major regulator of vascular tone because it releases vasoactive substances including: endothelium-derived relaxing factor (nitric oxide/EDRF), endothelium-derived hyperpolarizing factor (EDHF), prostacyclin, endothelin and endothelium-derived contracting factors (EDCFs). Three of these factors, nitric oxide, endothelin and a cyclooxygenase-dependent EDCF may play a role in congestive heart failure. A number of experimental and clinical studies describe impaired endothelium-dependent vasodilatations and increased plasma concentration of endothelin in congestive heart failure. The decrease of cardiac output, that results in a reduced shear stress on the endothelial cells and systemic endocrine compensatory mechanisms such as increased production of angiotensin-converting enzyme (leading to a greater breakdown of kinins) can modulate the release of nitric oxide and endothelin. It is unclear to which extent these modulations initiate, maintain, and/or compensate for the pathological process.
内皮是血管张力的主要调节者，因为它能释放血管活性物质，包括：内皮源性舒张因子（一氧化氮/内皮舒张因子）、内皮源性超极化因子、前列环素、内皮素和内皮源性收缩因子。其中三种因子，即一氧化氮、内皮素和一种环氧化酶依赖性内皮源性收缩因子可能在充血性心力衰竭中起作用。许多实验和临床研究描述了充血性心力衰竭中内皮依赖性血管舒张受损以及血浆内皮素浓度升高。心输出量减少会导致内皮细胞上的剪切应力降低，而全身内分泌代偿机制，如血管紧张素转换酶产生增加（导致激肽分解增加），可调节一氧化氮和内皮素的释放。目前尚不清楚这些调节在多大程度上启动、维持和/或补偿病理过程。
