Ascending myogenic autoregulation: interactions between tubuloglomerular feedback and myogenic mechanisms.
Ascending myogenic autoregulation: interactions between tubuloglomerular feedback and myogenic mechanisms.
复制标题
上行肌源性自动调节：肾小球反馈与肌源性机制之间的相互作用。
DOI：
10.1007/bf02460464
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发表时间：
1994
影响因子：
3.5
通讯作者：
Casellas,D
中科院分区：
文献类型：
--
作者：
Moore,LC;Rich,A;Casellas,D
采用肾血管和肾小管系统的数学模型来检验肾小管肾小球反馈（TGF）和肾脏肌源性自我调节机制之间可能发生协同相互作用的可能性。为了模拟成肌机制，我们用一个阻力网络来模拟肾脏血管，其中肾小球前总阻力随血管内压力而变化。此外，我们还建立了肾小球滤过、近端和亨氏袢重吸收以及传入小动脉阻力的tgf调节的稳态模型。结果表明，如果TGF作用于远端肾小球前血管，那么任何TGF诱导的血管收缩都会升高上游血管内压力，从而在更近端的血管段引发肌源性反应，这种现象被称为升肌源性（AMYO）反应。该模型进一步预测，AMYO反应的幅度可能与tgf诱导的传入阻力增加的幅度相似。因此，TGF激发对全肾血流动力学的影响可能远大于单个肾单位的测量结果。此外，肾灌注压升高的内在肌源性自身调节反应的很大一部分可能是TGF与肌源性机制之间的协同相互作用所致。
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 response in the more proximal vascular segments, a phenomenon referred to as an ascending 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 pedicted 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.