Effects of prolonged blockade of the renin angiotensin system on striated muscle microcirculation of spontaneously hypertensive rats.
Effects of prolonged blockade of the renin angiotensin system on striated muscle microcirculation of spontaneously hypertensive rats.
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长期阻断肾素血管紧张素系统对自发性高血压大鼠横纹肌微循环的影响。
DOI：
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发表时间：
1996
影响因子：
3.5
通讯作者：
H. Struijker
中科院分区：
文献类型：
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作者：
K. Scheidegger;J. Wood;H. van Essen;H. Struijker
微循环的改变在高血压的发生和维持中起着重要作用。这些变化可能是由于血管直径或小血管数量的改变。本研究采用背部微循环室模型，观察了不同的肾素-血管紧张素系统阻断剂对自发性高血压大鼠皮肤最大肌微循环的影响。动物用血管紧张素转换酶抑制剂（ACE抑制剂）苯那普利拉（3 mg/kg/d）或特异性血管紧张素II AT 1受体拮抗剂缬沙坦（3 mg/kg/d）治疗4周。两个治疗组的血压显著降低了22%至33%，降低程度相似，而对照组的血压继续升高。在用药前和用药期间测量微血管直径和密度，并与对照组进行比较。对于任何血管类型（小动脉或小静脉），与对照组相比，两种药物治疗对血管直径均无显著影响。与此相反，有一个显着的减少，小动脉和小静脉密度和大静脉密度治疗后的ACE抑制剂，而血管紧张素II AT 1受体拮抗剂没有显着的效果。这些数据并不表明血管紧张素II在长期控制横纹肌微血管张力中的作用。然而，血管紧张素II可能通过非AT 1受体介导的机制参与微血管生长，或者由ACE降解的其他血管活性肽可能有助于ACE抑制剂的作用。
Changes in microcirculation play an important role in the pathogenesis and maintenance of hypertension. The changes can be due to an alteration in vessel diameter or in the number of small blood vessels. In this study, the effects of prolonged administration of different blockers of the renin angiotensin system on the microcirculation of the cutaneous maximus muscle of young spontaneously hypertensive rats were determined by using the dorsal microcirculatory chamber model. Animals were treated with the angiotensin-converting enzyme inhibitor (ACE inhibitor) benazeprilat (3 mg/kg/d) or the specific angiotensin II AT1 receptor antagonist valsartan (3 mg/kg/d) for 4 weeks. Blood pressure was significantly lowered by 22 to 33% and to a similar extent in both treatment groups, whereas blood pressure in the control group continued to rise. Microvascular diameters and density were measured before and during the drug treatment and compared with those in the control group. There was no significant effect of either of the drug treatments on vascular diameters when compared with the control group for any vessel type (arterioles or venules). In contrast, there was a significant decrease in small arteriolar and venular density and in large venular density after treatment with the ACE inhibitor, whereas the angiotensin II AT1 receptor antagonist had no significant effect. The data do not suggest a role for angiotensin II in the long-term control of striated muscle microvascular tone. However, angiotensin II may be involved in microvascular growth via a non-AT1 receptor-mediated mechanism, or other vasoactive peptides degraded by ACE may contribute to the effects of the ACE inhibitor.