Decreased vascular relaxation in hypertension.
Decreased vascular relaxation in hypertension.
复制标题
高血压时血管舒张减少。
DOI：
--
复制
发表时间：
1976
影响因子：
3.5
通讯作者：
B. Berkowitz
中科院分区：
文献类型：
--
作者：
M. Cohen;B. Berkowitz
在自发性高血压大鼠和肾性高血压大鼠的血管中，双切口主动脉条的舒张作用减弱。在两种高血压模型中，环核苷酸和β肾上腺素能兴奋剂异丙肾上腺素均降低了主动脉舒张反应。使用其他两种血管扩张剂硝酸甘油和腺苷时也出现了主动脉舒张缺陷。通过测量暴露和随后去除血管收缩激动剂后的主动脉舒张，获得了高血压大鼠血管舒张能力降低的进一步证据。与京都Wistar血压正常大鼠的血管恢复时间相比，用去甲肾上腺素、5-羟色胺和氯化钾进行最大收缩后，自发性高血压大鼠的主动脉制备物放松至基线张力的时间显著延长。用利血平治疗自发性高血压大鼠，而不是肼苯哒嗪，导致主动脉制剂舒张能力的改善。基于这些数据，我们提出血管舒张功能的缺陷可能导致高血压，一些抗高血压药物可能改善或促进血管舒张。
Relaxation of spirally cut aortic strips was diminished in vessels from both spontaneously hypertensive rats and renal hypertensive rats. Aortic relaxation was decreased in response to the cyclic nucleotides and the beta adrenergic stimulant, isoproterenol, in both models, of hypertension. Defective aortic relaxation also occurred with two other vasodilators, nitroglycerin and adenosine. Further evidence for a reduced relaxant ability of blood vessels from hypertensive rats was obtained by measuring aortic relaxation after exposure and subsequent removal of vascular contractile agonists. The time for aortic preparations from spontaneously hypertensive rats to relax to base-line tension after maximum contraction with norepinephrine, serotonin and potassium chloride was significantly prolonged compared to recovery time for vessels from Kyoto Wistar normotensive rats. Treatment of the spontaneously hypertensive rat with reserpine, but not hydralazine, resulted in an improved ability of aortic preparations to relax. Based on these data, we propose that defects in vascular relaxation may contribute to hypertension and that some antihypertensive drugs may improve or facilitate vascular relaxation.