Spontaneously hypertensive rat resistance artery structure related to myogenic and mechanical properties
Spontaneously hypertensive rat resistance artery structure related to myogenic and mechanical properties
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DOI：
10.1042/cs20010036
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发表时间：
2001-10-01
期刊：
影响因子：
6
通讯作者：
Bund, SJ
中科院分区：
文献类型：
--
作者：
Bund, SJ
本文研究了体外加压条件下自发性高血压大鼠（SHRs）和Wistar-Kyoto （WKY）正常对照大鼠的动脉结构与肌源性（压力依赖性）收缩反应的关系。在被动和主动条件下，在5-200 mmHg的跨壁压力范围内，对两种菌株的股动脉和肠系膜抵抗动脉插管并加压，以确定压力-直径关系。在100mmhg放松条件下进行动脉几何测量。与WKY组相比，SHR组股骨动脉（5.00 +/- 0.44%，高于3.63 +/- 0.34%,P < 0.05）和肠系膜动脉（4.40 +/- 0.29%，高于2.62 +/- 0.23%,P < 0.001）中膜厚度/管腔直径（M/L）比值显著升高。SHR和WKY大鼠股骨动脉（分别为0.41 +/- 0.03和0.40 +/- 0.02）或肠系膜动脉（分别为0.56 +/- 0.02和0.63 +/- 0.03）的最大肌原性收缩，以最小归一化直径评估，无显著差异。动脉力学分析表明，与WKY大鼠相比，SHR肠系膜动脉的增量弹性模量降低，但SHR股动脉的增量弹性模量无显著差异。此外，SHR和WKY大鼠动脉在被动和主动条件下的估计体内压力下的壁应力相似。这些数据表明，SHRs引起的阻力动脉M/L比的增加与最大压力依赖性收缩反应的增加无关。SHRs引起的阻力动脉的M/L比增加并不是血管壁刚度增加的原因，但高血压相关的动脉几何异常在动脉压升高时起到了使壁应力正常化的作用。
This investigation related arterial structure to myogenic (pressure-dependent) contractile responses in resistance arteries from spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) normotensive control rats under pressurized conditions in vitro. Femoral and mesenteric resistance arteries from either strain were cannulated and pressurized in an arteriograph for the determination of pressure-diameter relationships under passive and active conditions in the range 5-200 mmHg transmural pressure. Arterial geometrical measurements were made under relaxed conditions at 100 mmHg. Media thickness/lumen diameter (M/L) ratios were significantly increased in SHR femoral (5.00 +/- 0.44% compared with 3.63 +/- 0.34%; P < 0.05) and mesenteric (4.40 +/- 0.29% compared with 2.62 +/- 0.23%; P < 0.001) arteries compared with those from WKY rats. Maximum myogenic contractions, assessed as minimum normalized diameters, were not significantly different in SHR and WKY rat femoral (0.41 +/- 0.03 and 0.40 +/- 0.02 respectively) or mesenteric (0.56 +/- 0.02 and 0.63 +/- 0.03 respectively) arteries. Arterial mechanical analyses demonstrated that incremental elastic modulus is reduced in SHR mesenteric arteries, but is not significantly different in SHR femoral arteries, compared with those from WKY rats. Additionally, wall stress at estimated in vivo pressures under passive and active conditions are similar in SHR and WKY rat arteries. These data demonstrate that increased M/L ratios in resistance arteries from SHRs are not associated with increased maximum pressure-dependent contractile responses. Increased M/L ratios in resistance arteries from SHRs are not accounted for by increased vessel wall stiffness, but the hypertension-associated arterial geometrical abnormalities act to normalize wall stress in the face of increased arterial pressure.