Impaired endothelium-dependent relaxations in rabbits subjected to aortic coarctation hypertension.
Impaired endothelium-dependent relaxations in rabbits subjected to aortic coarctation hypertension.
复制标题
患有主动脉缩窄高血压的兔子的内皮依赖性舒张受损。
DOI：
10.1161/01.hyp.10.2.164
复制
发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Mullane,KM
中科院分区：
文献类型：
--
作者：
Miller,MJ;Pinto,A;Mullane,KM
兔子因腹主动脉的肾上缩窄而患上高血压。 7天后，在取自高血压（胸主动脉、颈动脉）和正常血压（腹主动脉）区域的血管环中检查内皮依赖性和内皮非依赖性血管舒张。与假手术和完整对照相比，在暴露于血压升高的区域（即缩窄以上），去氧肾上腺素收缩环响应内皮依赖性激动剂（乙酰胆碱，A23187）的松弛受到损害。缩窄下方的腹主动脉对乙酰胆碱和 A23187 的反应没有改变。胸主动脉内皮依赖性反应的减弱并未受到环氧合酶抑制剂吲哚美辛预处理的影响。与乙酰胆碱和 A23187 相比，高血压区域的血管对不依赖内皮的激动剂硝普钠的反应并未减弱，表明缺陷发生在内皮。乙酰胆碱诱导的胸主动脉舒张的 EC50 与缩窄处的平均动脉压显着相关，表明内皮依赖性舒张受损的程度与血压升高的程度成正比。这项研究表明，内皮依赖性激动剂引起的舒张减弱是对血压升高的局部反应，而不是由于循环因素所致。
Rabbits were rendered hypertensive by suprarenal coarctation of the abdominal aorta. Seven days later, endothelium-dependent and endothelium-independent vascular relaxations were examined in vascular rings taken from hypertensive (thoracic aorta, carotid artery) and normotensive (abdominal aorta) regions. Relaxation of phenylephrine-contracted rings in response to endothelium-dependent agonists (acetylcholine, A23187) was impaired, compared with that in sham-operated and intact controls, in regions exposed to the elevated blood pressure (i.e., above the coarctation). Responses to acetylcholine and A23187 in the abdominal aorta, below the coarctation, were not altered. The diminished endothelium-dependent responses in the thoracic aorta were not affected by pretreatment with the cyclooxygenase inhibitor indomethacin. In contrast to acetylcholine and A23187, responses to the endothelium-independent agonist nitroprusside were not attenuated in vessels from hypertensive regions, indicating that the defect occurred in the endothelium. The EC50 for acetylcholine-induced relaxations of thoracic aorta correlated significantly with mean arterial pressure above the coarctation, indicating that the extent to which endothelium-dependent relaxation is impaired is in proportion to the degree of blood pressure elevation. This study suggests that the diminished relaxations by endothelium-dependent agonists is a local response to the elevation of blood pressure and is not due to a circulating factor.