Loutzenhiser Rodger, Bidani Anil, Chilton Lisa
Smooth Muscle Research Group, Department of Pharmacology and Therapeutics, The University of Calgary, Calgary, Alberta, Canada.
Circ Res. 2002 Jun 28;90(12):1316-24. doi: 10.1161/01.res.0000024262.11534.18.
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.
使用体外灌注的肾积水大鼠肾脏研究了传入小动脉肌源性反应的动力学特性。将描述压力依赖性血管收缩和舒张的时间过程以及直径稳态变化的方程结合起来,建立了自动调节的数学模型。通过使正弦压力波通过该模型构建传递函数。将这些结果与使用来自仪器化清醒大鼠的数据得出的结果进行比较。在每种情况下,在0.2至0.3Hz的频率下观察到增益降低和相位增加。然后我们研究了振荡压力信号的影响。该模型预测,在肌源性工作范围以上频率振荡的压力信号将引发持续的血管收缩,其幅度取决于峰值压力。这些预测在肾积水肾脏中得到了直接证实。在1至6Hz频率下呈现的压力振荡引发持续的传入血管收缩,反应幅度仅取决于峰值压力。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源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,而是暗示其在防止收缩压升高方面起主要作用。因此,传入小动脉的动力学特征允许该血管根据脉搏率时收缩压的变化来调节张力。我们认为该机制的主要功能是保护肾小球免受通常以脉搏频率存在的血压功率的影响。