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实验性高血压中的血管结构与平滑肌收缩性

Vascular structure and smooth muscle contractility in experimental hypertension.

作者信息

Mulvany M J

机构信息

Biophysics Institute, Aarhus University, Denmark.

出版信息

J Cardiovasc Pharmacol. 1987;10 Suppl 6:S79-85.

PMID:2485033
Abstract

The possible role of vascular structure as a pathogenetic factor in hypertension has been investigated by determining the media dimensions in resistance (mesenteric, renal, cerebral, and femoral) vessels taken from a variety of hypertensive rat models [spontaneously hypertensive (SHR), stroke-prone SHR (SHRSP), and one-kidney, one-clip renal hypertensive rats]. Resistance vessels from hybrid SHR/Wistar-Kyoto rats (WKYs) and from hybrid SHRSP/WKYs were also examined. In all cases, there was a correlation between media dimensions (media cross-sectional area or media/lumen ratio) of the resistance vessels (internal diameter of 100-300 microns) and the blood pressure of the rats concerned. Furthermore, the media of the SHR mesenteric resistance vessels were only increased in vessels larger than about 100 microns, indicating that structural changes were not to be expected in the microvasculature. These results suggest a causal relationship between blood pressure and the structure of the proximal resistance vasculature. Evidence that the increased structure is not solely a consequence of the increased pressure has been obtained from antihypertensive therapy experiments in which SHRs treated with hydralazine had resistance vessels with increased media/lumen ratios even though the animals had never become substantially hypertensive. The results point to a possible role for vascular structure in the development of hypertension.

摘要

通过测定取自多种高血压大鼠模型[自发性高血压大鼠(SHR)、易中风SHR(SHRSP)和单肾单夹肾性高血压大鼠]的阻力(肠系膜、肾、脑和股)血管的中膜尺寸,研究了血管结构作为高血压发病因素的可能作用。还检查了杂交SHR/威斯塔大鼠(WKY)和杂交SHRSP/WKY的阻力血管。在所有情况下,阻力血管(内径为100 - 300微米)的中膜尺寸(中膜横截面积或中膜/管腔比)与相关大鼠的血压之间存在相关性。此外,SHR肠系膜阻力血管的中膜仅在大于约100微米的血管中增加,这表明在微血管中不会出现结构变化。这些结果表明血压与近端阻力血管结构之间存在因果关系。从抗高血压治疗实验中获得了证据,证明结构增加并非仅仅是压力增加的结果,在这些实验中,用肼屈嗪治疗的SHR即使从未出现明显高血压,其阻力血管的中膜/管腔比也增加。结果表明血管结构在高血压发展中可能起作用。

相似文献

1
Vascular structure and smooth muscle contractility in experimental hypertension.实验性高血压中的血管结构与平滑肌收缩性
J Cardiovasc Pharmacol. 1987;10 Suppl 6:S79-85.
2
Role of vascular structure in blood pressure development of the spontaneously hypertensive rat.血管结构在自发性高血压大鼠血压形成中的作用。
J Hypertens Suppl. 1986 Oct;4(3):S61-3.
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Spontaneously hypertensive rat resistance artery structure related to myogenic and mechanical properties.自发性高血压大鼠阻力动脉结构与肌源性和力学特性的关系。
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Correlations and otherwise between blood pressure, cardiac mass and resistance vessel characteristics in hypertensive, normotensive and hypertensive/normotensive hybrid rats.高血压、正常血压及高血压/正常血压杂交大鼠的血压、心脏质量与阻力血管特征之间的相关性及其他关系。
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Structure and function of peripheral vascular smooth muscle in hypertension.高血压患者外周血管平滑肌的结构与功能
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Structural and functional adaptation in the rat myocardium and coronary vascular bed caused by changes in pressure and volume load.压力和容量负荷变化引起的大鼠心肌和冠状血管床的结构与功能适应性改变。
Acta Physiol Scand Suppl. 1985;540:1-47.
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Short-term treatment of spontaneously hypertensive rats with liver growth factor reduces carotid artery fibrosis, improves vascular function, and lowers blood pressure.用肝脏生长因子对自发性高血压大鼠进行短期治疗可减轻颈动脉纤维化、改善血管功能并降低血压。
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Enhanced expression of endothelin-1 gene may cause blood pressure-independent vascular hypertrophy.内皮素-1基因的表达增强可能导致不依赖血压的血管肥大。
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Influence of experimental reduction of media/lumen ratio on arterial myogenic properties of spontaneously hypertensive and Wistar-Kyoto rats.实验性降低中膜/管腔比值对自发性高血压大鼠和Wistar-Kyoto大鼠动脉肌源性特性的影响
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引用本文的文献

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Vascular Smooth Muscle Remodeling in Conductive and Resistance Arteries in Hypertension.高血压时传导和阻力动脉的血管平滑肌重塑。
Arterioscler Thromb Vasc Biol. 2018 Sep;38(9):1969-1985. doi: 10.1161/ATVBAHA.118.311229.
2
The effect of relaxants working through different transduction mechanisms on the tonic contraction produced in rat aorta by 4 beta-phorbol dibutyrate.通过不同转导机制起作用的松弛剂对4-β-佛波醇二丁酸酯在大鼠主动脉中产生的强直性收缩的影响。
Br J Pharmacol. 1989 Jul;97(3):647-56. doi: 10.1111/j.1476-5381.1989.tb12000.x.