Van de Voorde J, Vanheel B, Leusen I
Laboratory of Normal and Pathological Physiology, University of Gent, Belgium.
Pflugers Arch. 1988 May;411(5):500-4. doi: 10.1007/BF00582370.
Endothelium-dependent relaxation effects have been reported to be impaired in thoracic aorta from genetic and experimentally induced hypertensive rats. This study extends these observations to carotid artery and abdominal aorta from renovascular hypertensive rats. It was also found that rats with coarctation of aorta show depressed endothelium-dependent relaxation responses in thoracic aorta above the stenosis (high pressure region) while no depressed responses are observed in abdominal aorta below the stenosis (normal pressure region). Reversibility of the depression of endothelium-dependent relaxation was investigated on aorta from renovascular hypertensive rats in which blood pressure was normalized by removal of the stenotic kidney three months after induction of hypertension. Endothelium-dependent responses were restored partially after 1-2 weeks and completely after two months of normalization of blood pressure. These results indicate that the increased blood pressure is indeed the causative factor responsible for the impaired endothelium-dependent relaxations in arteries from experimental hypertensive rats, a phenomenon which is reversible, at least in our experimental conditions.
据报道，遗传性和实验性高血压大鼠胸主动脉的内皮依赖性舒张效应受损。本研究将这些观察结果扩展至肾血管性高血压大鼠的颈动脉和腹主动脉。还发现，主动脉缩窄大鼠的胸主动脉狭窄上方（高压区）的内皮依赖性舒张反应降低，而在狭窄下方的腹主动脉（正常压力区）未观察到反应降低。对肾血管性高血压大鼠的主动脉进行研究，以探讨内皮依赖性舒张降低的可逆性。在高血压诱导三个月后，通过切除狭窄肾脏使血压恢复正常。血压正常化1 - 2周后，内皮依赖性反应部分恢复，血压正常化两个月后完全恢复。这些结果表明，血压升高确实是实验性高血压大鼠动脉内皮依赖性舒张受损的致病因素，至少在我们的实验条件下，这一现象是可逆的。
