Gatzek W J
Med Hypotheses. 1978 May-Jun;4(3):221-30. doi: 10.1016/0306-9877(78)90004-x.
Observations which show that urine output can vary with changes in the contour of the pulse cure, that it can even increase while the mean blood pressure falls during counterpulsation, that the well known hypertensive effect of a renal artery stenosis can also be produced by an aneurysm of the renal artery, cannot be explained by orthodox concepts of renal hemodynamics. The anatomical fact that the afferent glomerular arteriole is about twice as large as the efferent has so far not been adequately explained. The hypothesis that the combination of pulsatile flow and the unique anatomical configuration of the glomerulus permit a hydraulic switching mechanism which modifies profoundly its perfusion explains these questions.
观察结果表明,尿量会随脉搏曲线形态的变化而改变,在反搏过程中,即使平均血压下降,尿量仍可能增加,肾动脉狭窄众所周知的高血压效应也可由肾动脉瘤产生,而传统的肾血流动力学概念无法解释这些现象。肾小球入球小动脉的管径约为出球小动脉的两倍这一解剖学事实,至今尚未得到充分解释。脉动血流与肾小球独特的解剖结构相结合,允许一种液压转换机制,该机制会深刻改变其灌注,这一假说解释了这些问题。