Kenney M J, Morgan D A
Department of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan 66506.
J Hypertens. 1994 Oct;12(10):1171-6.
Despite the return of mean arterial pressure (MAP) to control levels, aortic depressor nerve activity remains elevated from control levels after sustained phenylephrine-induced increases in MAP in spontaneously hypertensive rats (SHR) (Kenney MJ, Morgan DA, Mark AL: Am J Physiol 1990, 258:H1476-H1481). This suggests that sustained increases in arterial pressure may produce prolonged pressure-induced changes in afferent baroreceptor nerve activity in SHR. However, because phenylephrine can exert an excitatory effect on the aortic arch baroreceptors, the increase in aortic depressor nerve activity might have resulted from a persistent direct effect of phenylephrine. The aim of the current study was to determine whether elevations in MAP induced by aortic occlusion produce increases in aortic depressor nerve activity which persist after the return of MAP to control levels.
MAP and aortic depressor nerve activity were recorded before, during and after sustained (15-30 min) periods of aortic occlusion in SHR with intact adrenal glands (n = 18) and in adrenalectomized SHR (n = 10). Control experiments were completed in which the same variables were recorded before, during and after sham aortic occlusion in intact (n = 8) and adrenalectomized (n = 8) SHR.
Aortic occlusion increased MAP and aortic depressor nerve activity significantly from control levels. After aortic occlusion and the return of MAP to control levels, aortic depressor nerve activity remained significantly increased in 15 experiments, whereas in three experiments aortic depressor nerve activity was reduced. Aortic depressor nerve activity was increased significantly from control levels after aortic occlusion in adrenalectomized rats. Aortic depressor nerve activity remained unchanged from control levels after sham aortic occlusion in intact and adrenalectomized SHR.
Sustained elevations in MAP induce increases in aortic depressor nerve activity in intact and adrenalectomized SHR, which persist after the return of MAP to control levels. These observations suggest that sustained increases in arterial pressure may produce prolonged pressure-induced changes in afferent baroreceptor nerve activity in SHR.
尽管平均动脉压（MAP）恢复到对照水平，但在自发性高血压大鼠（SHR）中，在苯肾上腺素诱导MAP持续升高后，主动脉减压神经活动仍高于对照水平（Kenney MJ、Morgan DA、Mark AL：《美国生理学杂志》1990年，258：H1476 - H1481）。这表明动脉压的持续升高可能会使SHR传入压力感受器神经活动产生长期的压力诱导变化。然而，由于苯肾上腺素可对主动脉弓压力感受器产生兴奋作用，主动脉减压神经活动的增加可能是由苯肾上腺素的持续直接作用导致的。本研究的目的是确定主动脉阻断诱导的MAP升高是否会使主动脉减压神经活动增加，并在MAP恢复到对照水平后仍持续存在。
记录完整肾上腺的SHR（n = 18）和肾上腺切除的SHR（n = 10）在主动脉持续阻断（15 - 30分钟）期间及之后的MAP和主动脉减压神经活动。进行了对照实验，在完整（n = 8）和肾上腺切除（n = 8）的SHR中，记录假主动脉阻断期间及之后相同的变量。
主动脉阻断使MAP和主动脉减压神经活动显著高于对照水平。在主动脉阻断且MAP恢复到对照水平后，15次实验中主动脉减压神经活动仍显著增加，而在3次实验中主动脉减压神经活动降低。肾上腺切除大鼠在主动脉阻断后，主动脉减压神经活动较对照水平显著增加。完整和肾上腺切除的SHR在假主动脉阻断后，主动脉减压神经活动与对照水平相比无变化。
MAP的持续升高会使完整和肾上腺切除的SHR中主动脉减压神经活动增加，并在MAP恢复到对照水平后仍持续存在。这些观察结果表明，动脉压的持续升高可能会使SHR传入压力感受器神经活动产生长期的压力诱导变化。
