Andresen M C
Circ Res. 1984 Jun;54(6):750-9. doi: 10.1161/01.res.54.6.750.
In a variety of animal models, baroreceptor resetting during chronic hypertension has been correlated to vessel wall hypertrophy and decreased distensibility. In one possible mechanism of chronic resetting, termed the splinting hypothesis here, it has been suggested that a stiffer vessel wall might increase the minimum pressure required for activation of these mechanoreceptors (pressure threshold) and decrease suprathreshold pressure sensitivity. Lower vessel distensibility would alter baroreceptor function by preventing equivalent pressures from producing equivalent vessel distensions and, thus, receptor distortions. Recent studies have also suggested that the pressure threshold is strongly influenced by the most recent (minutes) history of blood pressure exposure during a process termed rapid resetting. Hypertension and advanced aging are associated with distensibility changes. The present study examines pressure and equivalent mechanical response characteristics of aortic baroreceptors from aged normotensive Wistar-Kyoto and spontaneously hypertensive rats. An in vitro aortic arch-aortic nerve preparation was used to assess the discharge properties from a number of baroreceptors and the pressure-diameter relationship of each aorta. Both control and rapid resetting protocols were used to study the baroreceptor characteristics. Aged Wistar-Kyoto rats were normotensive and averaged 115 weeks of age. Aged spontaneously hypertensive rats had systolic tail pressures of 187 mm Hg and averaged 76 weeks of age. Although aortic distensibility of aged WKYs was much lower than previously found in younger animals, the pressure threshold was unchanged. Aged spontaneously hypertensive rat receptors were chronically reset in proportion to their blood pressure. Decreased distensibility did not alter the rapid resetting process. It is concluded that baroreceptor pressure sensitivity is more closely related to aortic distensibility under several conditions altering vessel stiffness, whereas, the pressure threshold may be regulated additionally by mechanisms independent of distensibility. The results are inconsistent with the splinting hypothesis.
在多种动物模型中，慢性高血压期间压力感受器重置与血管壁肥厚及扩张性降低有关。在一种慢性重置的可能机制（此处称为夹板假说）中，有人提出更硬的血管壁可能会增加激活这些机械感受器所需的最小压力（压力阈值），并降低阈上压力敏感性。较低的血管扩张性会改变压力感受器功能，因为它会阻止同等压力产生同等的血管扩张，从而导致感受器变形。最近的研究还表明，在一个称为快速重置的过程中，压力阈值受最近（数分钟）血压暴露史的强烈影响。高血压和高龄与扩张性变化有关。本研究检查了老年正常血压的Wistar-Kyoto大鼠和自发性高血压大鼠主动脉压力感受器的压力及等效机械反应特性。采用体外主动脉弓-主动脉神经标本评估多个压力感受器的放电特性以及每条主动脉的压力-直径关系。使用对照和快速重置方案来研究压力感受器的特性。老年Wistar-Kyoto大鼠血压正常，平均年龄为115周。老年自发性高血压大鼠的尾动脉收缩压为187 mmHg，平均年龄为76周。尽管老年WKY大鼠的主动脉扩张性比之前在年轻动物中发现的要低得多，但压力阈值并未改变。老年自发性高血压大鼠的感受器根据其血压进行了慢性重置。扩张性降低并未改变快速重置过程。得出的结论是，在几种改变血管硬度的条件下，压力感受器压力敏感性与主动脉扩张性的关系更为密切，而压力阈值可能还受与扩张性无关的机制调节。结果与夹板假说不一致。
