Insulin and blood pressure: possible role of hemodynamics.

E Ferrannini
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引用次数: 26

Abstract

The association between hypertension and hyperinsulinemia/insulin resistance is well established but presently unexplained. Among several possible explanations, a connection between the two abnormalities can be envisioned at the level of the microvasculature in skeletal muscle. In fact, the insulin resistance of essential hypertension has been localized in skeletal muscle; in this tissue, on the other hand, rarefaction of the smaller arterioles can generate a rise in blood pressure. Thus, it is theoretically possible that structural changes in small vessels (caused by hypertension) may limit the diffusion of insulin and substrates from the intravascular space to the target cell surface. Alternatively, chronic hyperinsulinemia (caused by primary insulin resistance) could induce changes in small vessel walls (or their reactivity to pressor stimuli) capable of raising blood pressure. The details of these potential mechanisms are laid out within the framework of the hemodynamic phase of in vivo insulin action, and the available evidence bearing on them is discussed.

胰岛素和血压:血流动力学的可能作用。
高血压与高胰岛素血症/胰岛素抵抗之间的关系已得到证实,但目前尚未得到解释。在几种可能的解释中,可以在骨骼肌微血管水平上设想这两种异常之间的联系。事实上,原发性高血压的胰岛素抵抗已经局限于骨骼肌;另一方面,在这种组织中,小动脉的稀疏会导致血压升高。因此,从理论上讲,小血管的结构改变(由高血压引起)可能会限制胰岛素和底物从血管内空间向靶细胞表面的扩散。另外,慢性高胰岛素血症(由原发性胰岛素抵抗引起)可能引起小血管壁的改变(或其对压力刺激的反应性),从而升高血压。这些潜在机制的细节是在体内胰岛素作用的血流动力学阶段的框架内提出的,并讨论了与之相关的现有证据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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