Renal Myogenic Response: Kinetic Attributes and Physiological Role

R. Loutzenhiser, A. Bidani, L. Chilton
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引用次数: 249

Abstract

The kinetic attributes of the afferent arteriole myogenic response were investigated using the in vitro perfused hydronephrotic rat kidney. Equations describing the time course for pressure-dependent vasoconstriction and vasodilation, and steady-state changes in diameter were combined to develop a mathematical model of autoregulation. Transfer functions were constructed by passing sinusoidal pressure waves through the model. These findings were compared with results derived using data from instrumented conscious rats. In each case, a reduction in gain and increase in phase were observed at frequencies of 0.2 to 0.3 Hz. We then examined the impact of oscillating pressure signals. The model predicted that pressure signals oscillating at frequencies above the myogenic operating range would elicit a sustained vasoconstriction the magnitude of which was dependent on peak pressure. These predictions were directly confirmed in the hydronephrotic kidney. Pressure oscillations presented at frequencies of 1 to 6 Hz elicited sustained afferent vasoconstrictions and the magnitude of the response depended exclusively on the peak pressure. Elevated systolic pressure elicited vasoconstriction even if mean pressure was reduced. These findings challenge the view that the renal myogenic response exists to maintain glomerular capillary pressure constant, but rather imply a primary role in protecting against elevated systolic pressures. Thus, the kinetic features of the afferent arteriole allow this vessel to adjust tone in response to changes in systolic pressures presented at the pulse rate. We suggest that the primary function of this mechanism is to protect the glomerulus from the blood pressure power that is normally present at the pulse frequency.
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肾肌原性反应:动力学特性和生理作用
采用体外灌注肾积水大鼠肾脏,研究了传入小动脉肌生成反应的动力学特性。描述压力依赖性血管收缩和血管舒张的时间过程的方程,以及直径的稳态变化相结合,形成了一个自动调节的数学模型。传递函数是通过正弦压力波通过模型来构造的。这些发现与使用仪器的有意识大鼠的数据得出的结果进行了比较。在每种情况下,在0.2至0.3 Hz的频率下观察到增益减小和相位增加。然后,我们检查了振荡压力信号的影响。该模型预测,在高于肌源性操作范围的频率上振荡的压力信号将引起持续的血管收缩,其大小取决于峰值压力。这些预测在肾积水中得到了直接证实。频率为1 ~ 6hz的压力振荡引起持续的传入血管收缩,反应的大小完全取决于峰值压力。即使平均压力降低,收缩压升高也会引起血管收缩。这些发现挑战了肾肌原性反应的存在是为了维持肾小球毛细血管压力恒定的观点,而是暗示了在防止收缩压升高方面的主要作用。因此,传入小动脉的动力学特性允许该血管根据脉率呈现的收缩压变化来调整音调。我们认为,这种机制的主要功能是保护肾小球免受通常存在于脉频的血压功率的影响。
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