Chapleau M W, Abboud F M
Cardiovascular Center, University of Iowa College of Medicine, Iowa City 52242.
Circ Res. 1989 Sep;65(3):566-77. doi: 10.1161/01.res.65.3.566.
The threshold pressure of single baroreceptor units is decreased after compared with before exposure to pulsatile pressure according to previous studies in our laboratory. The purpose of the present study is to characterize the determinants of sensitization of arterial baroreceptors by pulsatile pressure. Carotid sinus nerve activity was recorded in dogs anesthetized with chloralose. Two indexes of baroreceptor "sensitivity" were obtained by comparing nerve activity before and immediately after exposure of the isolated carotid sinus to pulsatile pressure for periods up to 10 minutes. Sensitization occurred 1) when the threshold pressure of single baroreceptor units determined with a slow nonpulsatile ramp decreased after as compared with before pulsing and 2) when multiple unit activity increased after as compared with before pulsing at various mean levels of static pressure. Sensitization was evident after pulsing at mean pressure of 50 and 100 mm Hg, but not at 150 and 200 mm Hg, and was caused by the pulsatile change in diameter or deformation and not by the pulsatile change in wall tension. The magnitude of the effect was directly related to the duration of the pulsing period and to the frequency and amplitude of the pressure pulses. The sensitization could not be explained by increased diameter (sonomicrometers) or strain of the carotid sinus at the same pressure after pulsing; thus, there was an increase in "strain sensitivity" that outlasted the period of pulsing by up to several minutes. In most experiments the shift from static to pulsatile pressure at 50 and 100 mm Hg caused an increase in nerve activity, yet sensitization occurred after pulsing when one would have expected postexcitatory hyperpolarization or depression of activity upon return to static pressure. The sensitization was not caused by the release of prostacyclin from the endothelium since it was not reduced after endothelial denudation or inhibition of cyclooxygenase with indomethacin (30-80 microM) or ibuprofen (250 microM). We speculate that sensitization of baroreceptors by pulsatile pressure may contribute to the decreased sympathetic activity after periods of elevated pulse pressure (e.g., after exercise). We also propose that the decreased sensitivity of baroreceptors after acute elevation of arterial pressure (acute resetting) may be offset in part by the sensitizing effect of increased pulsatile stretch.
根据我们实验室之前的研究，与暴露于脉动压力之前相比，单个压力感受器单位的阈压力降低。本研究的目的是确定脉动压力引起动脉压力感受器敏化的决定因素。在以水合氯醛麻醉的犬中记录颈动脉窦神经活动。通过比较分离的颈动脉窦暴露于脉动压力长达10分钟之前和之后的神经活动，获得压力感受器“敏感性”的两个指标。当用缓慢的非脉动斜坡测定的单个压力感受器单位的阈压力在脉动后比脉动前降低时，以及当在各种平均静态压力水平下，多个单位活动在脉动后比脉动前增加时，敏化发生。在平均压力为50和100 mmHg时脉动后敏化明显，但在150和200 mmHg时不明显，并且是由直径的脉动变化或变形引起的，而不是由壁张力的脉动变化引起的。效应的大小与脉动期的持续时间、压力脉冲的频率和幅度直接相关。脉动后在相同压力下，颈动脉窦直径（超声测量仪）或应变增加并不能解释这种敏化；因此，“应变敏感性”增加，并且这种增加在脉动期之后持续长达几分钟。在大多数实验中，从50和100 mmHg的静态压力转变为脉动压力会导致神经活动增加，然而，当预期回到静态压力时会出现兴奋后超极化或活动抑制时，脉动后仍会发生敏化。敏化不是由内皮释放前列环素引起的，因为在内皮剥脱后或用吲哚美辛（30 - 80 microM）或布洛芬（250 microM）抑制环氧化酶后，敏化并未减弱。我们推测，脉动压力引起的压力感受器敏化可能有助于在脉压升高期（如运动后）后交感神经活动降低。我们还提出，动脉压急性升高后（急性重调定）压力感受器敏感性降低可能部分被增加的脉动牵张的敏化作用所抵消。
