肾素-血管紧张素-醛固酮系统:高血压管理的具体目标。
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堰先生,Dzau VJ
肾素-血管紧张素-醛固酮系统:高血压管理的具体目标。
J Hypertens。1999年12月,12 (12 Pt 3): 205 - 213年代。
- PubMed ID
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10619573 (在PubMed]
- 文摘
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血管紧张素ⅱ中起核心作用的规定系统性动脉压力通过其系统性通过肾素-血管紧张素-醛固酮合成级联。它直接作用于血管平滑肌作为一个强有力的血管收缩剂。此外,它会影响心脏收缩和心率在交感神经系统通过其行动。血管紧张素ⅱ也改变肾钠和水吸收通过它能够刺激肾上腺皮质球状带细胞的合成和分泌醛固酮。此外,它增强了口渴,刺激抗利尿激素的分泌。因此,血管紧张素ⅱ中起关键作用的急性和慢性监管通过其全身内分泌调节血压。强大的神经激素,调节全身动脉压,血管紧张素ⅱ也影响血管结构和功能通过旁分泌和自分泌的影响当地组织的合成。这种交替途径催化血管紧张素ⅱ生产的组织通过组织蛋白酶等酶G, chymostatin-sensitive血管紧张素酶II-generating, chymase。Intratissue血管紧张素ⅱ形成心血管重塑中起关键作用。Upregulation这些备用通道可能发生通过拉伸,血管内的压力、湍流。 Similar processes within the myocardium and glomeruli of the kidney may also lead to restructuring in these target organs, with consequent organ dysfunction. Additionally, angiotensin II may increase receptor density and sensitivity for other factors that modulate growth of vascular smooth muscle, such as fibroblast growth factor, transforming growth factor beta-1, platelet-derived growth factor, and insulin-like growth factors. Atherosclerosis may also be related, in part, to excessive angiotensin II effect on the vessel wall, which causes smooth muscle cell growth and migration. It also activates macrophages and increases platelet aggregation. Angiotensin II stimulates plasminogen activator inhibitor 1 and directly causes endothelial dysfunction. Other postulated effects of angiotensin II on vascular structure that could promote atherogenesis include inhibition of apoptosis, increase in oxidative stress, promotion of leukocyte adhesion and migration, and stimulation of thrombosis. Inhibition of angiotensin II synthesis with an angiotensin-converting enzyme inhibitor has been demonstrated to be beneficial in modifying human disease progression. This is clearly apparent in clinical trials involving patients with diabetic nephropathy, postmyocardial infarction, or advanced degrees of systolic heart failure. Thus, angiotensin II is an excellent target for pharmacologic blockade. Not only does it play a pivotal role in both the acute and chronic regulation of systemic arterial pressure, but it also is an important modulator of cardiovascular structure and function and may be specifically involved in disease progression. Modification of angiotensin II effect may therefore serve a dual purpose. Not only will blood pressure reduction occur with less stretch, stress, and turbulence of the vascular wall, but there will also be less stimulation, either directly or indirectly, for restructuring and remodeling of the cardiovascular tree.