Franco Guevara M, Navar L G, Herrera-Acosta J, Bell D
Departamento de Nefrología, Instituto Nacional de Cardiología Ignacio Chávez, México.
Gac Med Mex. 1994 May-Jun;130(3):139-45; discussion 146-7.
The tubuloglomerular feedback system (TGF), the main component of the autoregulation mechanism, maintains constant glomerular blood flow and filtration rate. The system is based in the morpho-functional association among the macula densa, the afferent and efferent arterioles, the glomerulus and the extraglomerular mesangial cells. The macula densa cells sense the changes in solute concentrations and osmolarity in the tubular fluid and send vasoconstrictor or vasodilatory signals to the arterioles that modify blood flow and glomerular filtration rate. However, the mechanism by which the macula densa sends signals to the arterioles remains unknown. A chemical mediator such as prostaglandins or adenosine has been postulated. Our studies discarded the participation of prostaglandins as mediators. Further studies from our group with adenosine analogs indicate that this nucleotide participates in the activation of the TGF responses, and suggest alternate activation pathways not previously described. To evaluate the role of TGF feedback in the glomerular hemodynamic changes associated with progression of renal damage, we studied TGF responses in rats with Goldblatt hypertension and partial ablation of the contralateral kidney. Our results suggest that the sensitivity of the system is decreased. This alteration may contribute to glomerular hypertension and progression to renal damage.
球管反馈系统（TGF）是自身调节机制的主要组成部分，可维持肾小球血流量和滤过率恒定。该系统基于致密斑、入球和出球小动脉、肾小球及球外系膜细胞之间的形态功能联系。致密斑细胞感知肾小管液中溶质浓度和渗透压的变化，并向小动脉发送血管收缩或舒张信号，从而改变血流量和肾小球滤过率。然而，致密斑向小动脉发送信号的机制尚不清楚。有人提出一种化学介质，如前列腺素或腺苷。我们的研究排除了前列腺素作为介质的作用。我们小组对腺苷类似物的进一步研究表明，这种核苷酸参与了TGF反应的激活，并提示了以前未描述的替代激活途径。为了评估TGF反馈在与肾损伤进展相关的肾小球血流动力学变化中的作用，我们研究了患有Goldblatt高血压和对侧肾脏部分切除的大鼠的TGF反应。我们的结果表明该系统的敏感性降低。这种改变可能导致肾小球高血压和肾损伤进展。
