EVIDENCE FOR INCREASED MEDIA THICKNESS, INCREASED NEURONAL AMINE UPTAKE, AND DEPRESSED EXCITATION CONTRACTION COUPLING IN ISOLATED RESISTANCE VESSELS FROM ESSENTIAL HYPERTENSIVES
EVIDENCE FOR INCREASED MEDIA THICKNESS, INCREASED NEURONAL AMINE UPTAKE, AND DEPRESSED EXCITATION CONTRACTION COUPLING IN ISOLATED RESISTANCE VESSELS FROM ESSENTIAL HYPERTENSIVES
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DOI：
10.1161/01.res.61.2.181
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发表时间：
1987-08-01
影响因子：
20.1
通讯作者：
MULVANY, MJ
中科院分区：
文献类型：
--
作者：
AALKJAER, C;HEAGERTY, AM;MULVANY, MJ
研究了离体皮下阻力血管（约170亩）的功能和形态特征。对15名未经治疗的原发性高血压患者和15名匹配的对照组进行了检查。高血压患者的血管中膜厚度与管腔直径之比增加29%。高血压患者血管对去甲肾上腺素（NA）的最大力发展表现为主动压力（血管在体内可能收缩的压力的估计）高出30%，而主动介质应力（每平方单位平滑肌的力）和对NA的敏感性没有显著差异。血管加压素、血清素、血管紧张素II和K+的活性介质压力和敏感性均升高。然而，高血压患者血管中可卡因（一种神经元胺泵抑制剂）对NA敏感性的左移增强[pD2（+可卡因）和pD2（-可卡因）为0.185 .+-]。0.053和0.040 .+-。0.044，高血压和正常血压组，p < 0.05]提示原发性高血压患者突触前功能异常。此外，钙敏感性降低（pD2为4.197 +-）。0.050和4.381 .+-。高血压患者血管舒张速率更快（p < 0.05），表明高血压患者的兴奋-收缩耦合可能受到抑制。结果表明，原发性高血压患者的升压反应增加在很大程度上可以通过血管结构改变来解释，而平滑肌功能要么不变，要么可能受到抑制。
The functional and morphologic characteristics of isolated subcutaneous resistance vessels (about 170 .mu.m i.d.) from 15 untreated subjects with essential hypertension and 15 matched controls were examined. The vessels from the hypertensives had a 29% increase in the media-thickness-to-lumen-diameter ratio. The maximal force development to noradrenaline (NA) expressed as active pressure (an estimate of the pressure the vessels could have contracted against in vivo) was 30% higher in vessels from the hypertensives, while active media stress (force per square unit of smooth muscle) and sensitivity to NA was not significantly different. Increased active pressure, as well as unaltered active media stress and sensitivity, was seen for vasopressin, serotonin, angiotensin II, and K+. There was, however, an enhanced leftward shift of the NA sensitivity with cocaine (an inhibitor of the neuronal amine pump) in vessels from the hypertensives [pD2(+cocaine) and pD2(-cocaine) were 0.185 .+-. 0.053 and 0.040 .+-. 0.044, hypertensives and normotensives, respectively, p < 0.05] suggesting an abnormality of presynaptic function in essential hypertension. Furthermore, the calcium sensitivity was depressed (pD2 was 4.197 .+-. 0.050 and 4.381 .+-. 0.068, hypertensives and normotensives, respectively, p < 0.05), and the rate of relaxation was faster (p < 0.05) in vessels from hypertensives, suggesting that excitation-contraction coupling might be depressed. The results suggest that the increased pressor response in essential hypertension can, to a large extent, be explained by altered vascular structure, while smooth muscle function is either unchanged or possibly depressed.