Coleridge H M, Coleridge J C, Poore E R, Roberts A M, Schultz H D
J Physiol. 1984 May;350:309-26. doi: 10.1113/jphysiol.1984.sp015203.
In order to throw light on the mechanism of acute hypertensive baroreceptor resetting, we examined the relationship between aortic baroreceptor firing and aortic wall properties in anaesthetized dogs as pressure was varied in a number of ways. We recorded baroreceptor impulses from the left aortic nerve, and measured aortic pressure with a catheter-tip transducer and external aortic diameter with ultrasonic transit-time transducers. Narrow anticlockwise hysteresis loops were evident in the pressure-diameter relationship of the upper thoracic aorta, both during the rapid pulsatile pressure changes of the cardiac cycle and during the slow excursions of mean pressure imposed for construction of baroreceptor pressure--response curves. In contrast to the 'phase-lag' response of diameter to pressure, the baroreceptor response was 'phaselead' in character, decreasing when stress-induced creep occurred in the aortic wall. When the mean arterial pressure set-point was increased from 100 to 125 mmHg for 20 min, the hysteresis loops relating mean diameter to mean pressure in the range 60-200 mmHg were displaced along the diameter axis in the direction of wall creep. A reduction in the baroreceptor response to pressure (i.e. resetting) always accompanied this displacement. Administration of ouabain (25-35 micrograms/kg) had no consistent effect on baroreceptor resetting. It has been suggested that acute baroreceptor resetting is akin to adaptation. To investigate the possibility that the two processes are accompanied by similar changes in aortic wall properties, we converted the aorta into a closed sac and distended it with a square wave of pressure. Like resetting, adaptation of the baroreceptor response to maintained pressure was associated with a small degree of creep of the aortic wall. Our results are compatible with the hypothesis that acute hypertensive resetting of aortic baroreceptors is similar to adaptation, both phenomena being attributable to relaxation of viscoelastic coupling elements, leading to a reduction of strain at the receptor membrane. Whether viscoelastic processes alone can account for acute resetting, or whether changes in ionic balance are involved also, baroreceptor responsiveness is a function of the stress history of the wall, the pressure-response curve moving along the pressure axis in the direction of the prevailing set-point. Hence, in early hypertension physiological resetting of baroreceptors will precede pathological resetting, and may even promote an upward movement of set-point.
为了阐明急性高血压压力感受器重调定的机制，我们以多种方式改变压力，研究了麻醉犬主动脉压力感受器放电与主动脉壁特性之间的关系。我们记录了左主动脉神经的压力感受器冲动，并用导管尖端换能器测量主动脉压力，用超声渡越时间换能器测量主动脉外径。在心动周期快速的搏动性压力变化期间以及为构建压力感受器压力 - 反应曲线而施加的平均压力缓慢变化期间，胸段主动脉上部的压力 - 直径关系中均出现明显的逆时针窄滞后环。与直径对压力的“相位滞后”反应不同，压力感受器的反应具有“相位超前”的特征，当主动脉壁出现应力诱导的蠕变时，反应会降低。当平均动脉压设定点从100 mmHg升高至125 mmHg并持续20分钟时，在60 - 200 mmHg范围内将平均直径与平均压力相关联的滞后环沿直径轴朝着壁蠕变的方向移位。压力感受器对压力的反应降低（即重调定）总是伴随着这种移位。给予哇巴因（25 - 35微克/千克）对压力感受器重调定没有一致的影响。有人提出急性压力感受器重调定类似于适应过程。为了研究这两个过程是否伴随着主动脉壁特性的类似变化，我们将主动脉转变为一个封闭囊，并通过方波压力使其扩张。与重调定一样，压力感受器对持续压力的适应与主动脉壁的小程度蠕变有关。我们的结果与以下假设相符：主动脉压力感受器的急性高血压重调定类似于适应，这两种现象均归因于粘弹性耦合元件的松弛，导致感受器膜处应变降低。无论是仅粘弹性过程就能解释急性重调定，还是离子平衡的变化也参与其中，压力感受器的反应性都是壁应力历史的函数，压力 - 反应曲线沿压力轴朝着当前设定点的方向移动。因此，在早期高血压中，压力感受器的生理重调定将先于病理重调定，甚至可能促进设定点的上升。
