Ferrannini E
Metabolism Unit of the C.N.R. Institute of Clinical Physiology, Pisa, Italy.
Clin Exp Hypertens A. 1992;14(1-2):271-84. doi: 10.3109/10641969209036188.
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.
高血压与高胰岛素血症/胰岛素抵抗之间的关联已得到充分证实,但目前尚无合理解释。在几种可能的解释中,可以设想这两种异常情况在骨骼肌微血管水平上存在联系。事实上,原发性高血压的胰岛素抵抗已定位在骨骼肌;另一方面,在该组织中,较小动脉的稀疏可导致血压升高。因此,理论上小血管的结构变化(由高血压引起)可能会限制胰岛素和底物从血管内空间扩散到靶细胞表面。或者,慢性高胰岛素血症(由原发性胰岛素抵抗引起)可能会诱导小血管壁发生变化(或其对升压刺激的反应性),从而导致血压升高。这些潜在机制的细节在体内胰岛素作用的血流动力学阶段框架内进行阐述,并讨论了与之相关的现有证据。