Department of Physiology and Anatomy, Human Vascular Physiology Laboratory, University of North Texas Health Science Center, Ft. Worth, Texas.
Department of Surgery, University of North Texas Health Science Center, Ft. Worth, Texas.
Am J Physiol Heart Circ Physiol. 2020 Apr 1;318(4):H976-H984. doi: 10.1152/ajpheart.00019.2020. Epub 2020 Mar 6.
There is a sustained reduction in arterial blood pressure that occurs in aged adults following exposure to acute leg heating. We tested the hypothesis that acute leg heating would decrease arterial blood pressure in aged adults secondary to sympathoinhibition. We exposed 13 young and 10 aged adults to 45 min of leg heating. Muscle sympathetic nerve activity (radial nerve) was measured before leg heating (preheat) and 30 min after (recovery) and is expressed as burst frequency. Neurovascular transduction was examined by assessing the slope of the relation between muscle sympathetic nerve activity and leg vascular conductance measured at rest and during isometric handgrip exercise performed to fatigue. Arterial blood pressure was well maintained in young adults (preheat, 86 ± 6 mmHg vs. recovery, 88 ± 7 mmHg; = 0.4) due to increased sympathetic nerve activity (preheat, 16 ± 7 bursts/min vs. recovery, 22 ± 10 bursts/min; < 0.01). However, in aged adults, sympathetic nerve activity did not differ from preheat (37 ± 5 bursts/min) to recovery (33 ± 6 bursts/min, = 0.1), despite a marked reduction in arterial blood pressure (preheat, 101 ± 7 mmHg vs. recovery, 94 ± 6 mmHg; < 0.01). Neurovascular transduction did not differ from preheat to recovery for either age group ( ≥ 0.1). The reduction in arterial blood pressure that occurs in aged adults following exposure to acute leg heating is mediated, in part, by a sympathoinhibitory effect that alters the compensatory neural response to hypotension. There is a sustained reduction in arterial blood pressure that occurs in aged adults following exposure to acute leg heating. However, the neurovascular mechanisms mediating this response remain unknown. Our findings demonstrate for the first time that this reduction in arterial blood pressure is mediated, in part, by a sympathoinhibitory effect that alters the compensatory neural response to hypotension in aged adults.
在急性腿部加热后，老年成年人的动脉血压持续下降。我们测试了以下假设：急性腿部加热会通过交感神经抑制导致老年成年人的动脉血压下降。我们让 13 名年轻成年人和 10 名老年成年人暴露在 45 分钟的腿部加热中。在腿部加热前（预热）和 30 分钟后（恢复）测量桡神经的肌肉交感神经活动，并以爆发频率表示。通过评估在休息和疲劳时进行的等长握力运动期间肌肉交感神经活动与腿部血管传导之间的关系的斜率来检查神经血管转导。由于交感神经活动增加，年轻成年人的动脉血压保持良好（预热时为 86±6mmHg，恢复时为 88±7mmHg； = 0.4）（预热时为 16±7 次/分钟，恢复时为 22±10 次/分钟； < 0.01）。然而，在老年成年人中，尽管动脉血压明显下降（预热时为 101±7mmHg，恢复时为 94±6mmHg； < 0.01），但与预热时相比，交感神经活动没有差异（37±5 次/分钟，33±6 次/分钟， = 0.1）。神经血管转导在两个年龄组中从预热到恢复都没有差异（ ≥ 0.1）。急性腿部加热后老年成年人动脉血压的降低部分是通过交感神经抑制作用介导的，这种作用改变了对低血压的代偿性神经反应。在急性腿部加热后，老年成年人的动脉血压持续下降。然而，介导这种反应的神经血管机制仍不清楚。我们的发现首次表明，这种动脉血压的降低部分是通过交感神经抑制作用介导的，这种作用改变了老年成年人对低血压的代偿性神经反应。
