Aukland K
Department of Physiology, University of Bergen, Norway.
J Hypertens Suppl. 1989 Sep;7(4):S71-6; discussion S77.
Myogenic mechanisms in the kidney are part of the autoregulation mechanism which maintains a constant renal blood flow at varying arterial pressure. Concomitant autoregulation of glomerular pressure and filtration indicates regulation of preglomerular resistance. Model and experimental studies were performed to evaluate two mechanisms in the kidney, myogenic response and tubuloglomerular feedback. A mathematical model showed good autoregulation through a myogenic response, aimed at maintaining a constant wall tension in each segment of the preglomerular vessels. Tubuloglomerular feedback gave rather poor autoregulation. The myogenic mechanism showed 'descending' resistance changes, starting in the larger arteries, and successively affecting downstream preglomerular vessels at increasing arterial pressures. This finding was supported by micropuncture measurements of pressure in the terminal interlobular arteries. Evidence that the mechanism was myogenic was obtained by exposing the kidney to a subatmospheric pressure of 40 mmHg; this led to an immediate increase in renal resistance, which could not be prevented by denervation or various blocking agents.
肾脏中的肌源性机制是自动调节机制的一部分,该机制可在不同动脉压下维持恒定的肾血流量。肾小球压力和滤过的伴随自动调节表明了肾小球前阻力的调节。进行了模型和实验研究以评估肾脏中的两种机制,即肌源性反应和肾小管-肾小球反馈。一个数学模型显示通过肌源性反应可实现良好的自动调节,旨在维持肾小球前血管各节段的恒定壁张力。肾小管-肾小球反馈的自动调节效果较差。肌源性机制显示出“下行性”阻力变化,始于较大动脉,并在动脉压升高时依次影响下游的肾小球前血管。小叶间终末动脉压力的微穿刺测量结果支持了这一发现。通过将肾脏暴露于40 mmHg的低于大气压的压力下,获得了该机制为肌源性的证据;这导致肾阻力立即增加,而去神经支配或各种阻滞剂无法阻止这种增加。