Moore L C, Rich A, Casellas D
Department of Physiology and Biophysics, State University of New York, Stony Brook 11794.
Bull Math Biol. 1994 May;56(3):391-410. doi: 10.1007/BF02460464.
A mathematical model of the renal vascular and tubular systems was used to examine the possibility that synergistic interactions might occur between the tubuloglomerular feedback (TGF) and myogenic autoregulatory mechanisms in the kidney. To simulate the myogenic mechanism, the renal vasculature was modelled with a resistance network where the total preglomerular resistance varies with intravascular pressure. In addition, a steady-state model of glomerular filtration, proximal and Henle's loop reabsorption, and TGF-modulation of afferent arteriolar resistance was derived. The results show that, if TGF acts on the distal portion of the preglomerular vasculature, then any TGF-induced vasoconstriction should raise upstream intravascular pressure and, thereby, trigger a myogenic (AMYO) response. The model further predicts that the magnitude of the AMYO response can be similar in magnitude to the TGF-induced increment in afferent resistance. Hence, the effects of TGF excitation on whole kidney hemodynamics may be much greater than predicted from measurements in single nephrons. Moreover, a significant fraction of the intrinsic myogenic autoregulatory response to increased renal perfusion pressure may result from a synergistic interaction between the TGF and myogenic mechanisms.
利用肾脏血管和肾小管系统的数学模型来研究肾小管-肾小球反馈(TGF)与肾脏肌源性自动调节机制之间可能发生协同相互作用的可能性。为了模拟肌源性机制,用一个阻力网络对肾血管系统进行建模,其中肾小球前总阻力随血管内压力变化。此外,还推导了肾小球滤过、近端小管和髓袢重吸收以及TGF对入球小动脉阻力调节的稳态模型。结果表明,如果TGF作用于肾小球前血管系统的远端部分,那么任何由TGF诱导的血管收缩都应升高上游血管内压力,从而触发肌源性(AMYO)反应。该模型进一步预测,AMYO反应的幅度在大小上可能与TGF诱导的入球阻力增加相似。因此,TGF兴奋对全肾血流动力学的影响可能比单肾单位测量所预测的要大得多。此外,对肾灌注压升高的固有肌源性自动调节反应的很大一部分可能是由TGF和肌源性机制之间的协同相互作用引起的。