ATP mediates tubuloglomerular feedback.
ATP mediates tubuloglomerular feedback.
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ATP 介导肾小球反馈。
DOI：
10.1152/ajpregu.00071.2002
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Navar,LGabriel
中科院分区：
文献类型：
--
作者：
Nishiyama,Akira;Navar,LGabriel
黄斑Densa细胞构成了肾小管球球反馈(TGF)机制的传感组件，通过向传入小动脉传递信号来对肾小管液成分的变化作出反应，从而调节肾小球前血管阻力和对肾小管(14、15)的过滤负荷。这一有趣的机制仍在深入研究中，越来越多的证据表明，致密斑细胞和血管平滑肌细胞之间的通讯通路涉及多种相互作用的旁分泌因子。致密斑细胞被认为产生和释放三磷酸腺苷、腺苷、花生四烯酸代谢物和一氧化氮。其中一些用于调节转化生长因子机制的敏感性，区分对远端肾小管液成分急剧变化做出反应的强大的调节剂和特定的介质仍然是一个艰巨的挑战。也许区分介质和调节物的最重要的标准是在致密黄斑刺激的变化和与肾血管阻力(RVR)变化相关的转化生长因子介质的释放或浓度的变化之间存在直接的关系。由于转化生长因子机制参与小动脉血管对灌流压变化的自身调节反应，人们也认识到转化生长因子机制的介质对与自身调节反应相关的RVR的变化起作用(15，20，22)。因此，人们可以期待关于调节转化生长因子机制和调节自身调节反应的机制的证据有一定的内部一致性。考虑到转化生长因子机制是肾脏自身调节反应的主要介体，并且主要用于调节传入小动脉阻力(9，15，20)，令人惊讶的是，关于致密斑区功能与传入小动脉阻力变化之间的信号机制的性质尚未达成共识。
THE MACULA DENSA CELLS COMPRISE the sensing component of the tubuloglomerular feedback (TGF) mechanism and respond to changes in tubular fluid composition by transmitting signals to the afferent arterioles thus regulating the preglomerular vascular resistance and filtered load to the tubules (14, 15). This intriguing mechanism has remained under intensive investigation, and the accrued evidence indicates that there are multiple interacting paracrine agents involved in the communication pathway between the macula densa cells and the vascular smooth muscle cells. The macula densa cells are thought to produce and release ATP, adenosine, arachidonic acid metabolites, and nitric oxide. Some of these serve to modulate the sensitivity of the TGF mechanism, and it has remained a formidable challenge to discriminate between the powerful modulators and the specific mediator that respond to the acute changes in distal tubular fluid composition. Perhaps the single most important criterion distinguishing between the mediator and modulators is that there should be a direct relationship between the change in the macula densa stimulus and the change in the release or concentration of the TGF mediator associated with the change in renal vascular resistance (RVR).Because the TGF mechanism participates in the autoregulatory responses of the arteriolar vasculature to changes in perfusion pressure, it is also recognized that the mediator of the TGF mechanism contributes to the changes in RVR associated with autoregulatory responses (15, 20, 22). Thus one would expect a certain internal consistency in the evidence regarding the mechanism that mediates the TGF mechanism and the mechanism that mediates autoregulatory responses. Considering that the TGF mechanism is a major mediator of renal autoregulatory responses and primarily serves to regulate afferent arteriolar resistance (9, 15, 20), it is surprising that no consensus has emerged regarding the nature of the signaling mechanism that links macula densa function with the changes in affer-