Feldberg R, Colding-Jørgensen M, Holstein-Rathlou N H
Physics Department, Technical University of Denmark, Lyngby, Denmark.
Am J Physiol. 1995 Oct;269(4 Pt 2):F581-93. doi: 10.1152/ajprenal.1995.269.4.F581.
The present study investigates the interaction between the tubuloglomerular feedback (TGF) response and the myogenic mechanism by use of a mathematical model. The two control mechanisms are implemented in a spatially distributed model of the rat renal juxtamedullary afferent arteriole. The model of the afferent arteriole is based on in vivo measurements of the stress-strain relation in muscle strips. Analysis of experimental data shows that the myogenic response can be modeled by a linear relation between the transmural pressure and the level of activation of the vascular smooth muscle cells. The contribution of TGF to smooth muscle activity is assumed to be a linear function of the glomerular capillary pressure. The results show that the myogenic response plays an important role in renal blood flow autoregulation. Without a myogenic response, mechanisms such as TGF that are localized in the distal segments of the microvasculature would not be able to achieve autoregulation because of passive, pressure-mediated effects in the upstream vascular segments. In addition, it is shown that a strong myogenic response may lead to both propagation and enhancement of vascular effects mediated through mechanisms located in the distal part of the afferent arteriole. An ascending myogenic response could enhance the regulatory efficiency of the TGF mechanism by increasing the open-loop gain of the system. However, such a synergistic interaction will only be observed when the two mechanisms operate on more or less separate segments of the afferent arteriole. In the case where they operate on common segments of the arteriole, the outcome of the interaction may well be antagonistic.
本研究通过使用数学模型来探究肾小管-肾小球反馈(TGF)反应与肌源性机制之间的相互作用。这两种控制机制在大鼠肾近髓传入小动脉的空间分布模型中得以实现。传入小动脉模型基于对肌条应力-应变关系的体内测量。对实验数据的分析表明,肌源性反应可以通过跨壁压力与血管平滑肌细胞激活水平之间的线性关系来建模。TGF对平滑肌活动的贡献被假定为肾小球毛细血管压力的线性函数。结果表明,肌源性反应在肾血流自动调节中起重要作用。如果没有肌源性反应,诸如TGF等位于微血管远端段的机制将无法实现自动调节,因为上游血管段存在被动的压力介导效应。此外,研究表明,强烈的肌源性反应可能导致通过位于传入小动脉远端的机制介导的血管效应的传播和增强。上行性肌源性反应可通过增加系统的开环增益来提高TGF机制的调节效率。然而,只有当这两种机制在传入小动脉的或多或少不同的段上起作用时,才会观察到这种协同相互作用。在它们作用于小动脉的共同段的情况下,相互作用的结果很可能是拮抗的。