Shimokawa H
The Research Institute of Angiocardiology and Cardiovascular Clinic, Kyushu University School of Medicine, Fukuoka, Japan.
J Atheroscler Thromb. 1998;4(3):118-27. doi: 10.5551/jat1994.4.118.
The endothelium modulates the tone of the underlying vascular smooth muscle by releasing relaxing factors, including prostacyclin, nitric oxide (NO), and endothelium-derived hyperpolarizing factor (EDHF). In most types of hypertension, endothelium-dependent relaxations are impaired because of a reduced production and/or action of endothelium-derived NO and EDHF. In essential hypertension, endothelium-dependent relaxations are reduced because of a concomitant release of vasoconstrictor prostanoids (endoperoxides and thromboxane A2). These prostanoids may be produced in the vascular smooth muscle rather than in the endothelium. The endothelial dysfunction observed in hypertension is likely to be a consequence rather than a cause of the disease, representing premature aging of the blood vessels due to the chronic exposure to the high blood pressure. The endothelial dysfunction can be improved by antihypertensive therapy, favoring the prevention of the occurrence of vascular complications in hypertension.
内皮细胞通过释放舒张因子来调节其下的血管平滑肌张力,这些舒张因子包括前列环素、一氧化氮(NO)和内皮衍生超极化因子(EDHF)。在大多数类型的高血压中,由于内皮衍生的NO和EDHF产生减少和/或作用受损,内皮依赖性舒张功能受损。在原发性高血压中,由于血管收缩性前列腺素(内过氧化物和血栓素A2)的同时释放,内皮依赖性舒张功能降低。这些前列腺素可能在血管平滑肌而非内皮细胞中产生。高血压中观察到的内皮功能障碍可能是该疾病的结果而非病因,代表了由于长期暴露于高血压导致的血管过早老化。抗高血压治疗可改善内皮功能障碍,有助于预防高血压患者发生血管并发症。