ROLE OF ADENOSINE IN THE SYMPATHETIC ACTIVATION PRODUCED BY ISOMETRIC-EXERCISE IN HUMANS

ROLE OF ADENOSINE IN THE SYMPATHETIC ACTIVATION PRODUCED BY ISOMETRIC-EXERCISE IN HUMANS
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DOI:
10.1172/jci117147
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发表时间:
1994-04-01
影响因子:
15.9
通讯作者:
BIAGGIONI, I
BIAGGIONI, I
中科院分区:
医学1区
文献类型:
--
作者:
COSTA, F;BIAGGIONI, I

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等长运动会增加交感神经活动和血压。这种运动按压反射部分是由激活肌肉传入神经(代谢感受器)的代谢产物介导的。尽管腺苷是一种已知的抑制性神经调节剂,但越来越多的证据表明它可以激活传入神经。因此,我们研究了腺苷刺激肌肉传入并参与健康志愿者的运动按压反射的假设。在静脉阻塞期间将腺苷注射到前臂,以防止全身效应,模拟运动反应,在所有研究剂量(2、3和4毫克)下增加肌肉交感神经活动(MSNA,下肢显微神经造影)和平均动脉血压(MABP)。仅在最高剂量时心率才会增加。臂内腺苷 (4 mg) 使 MSNA 增加 96+/-25% (n = 6, P < 0.01),使 MABP 增加 12+/-3 mmHg (P < 0.01)。腺苷会引起前臂不适,但同等疼痛刺激(前臂缺血和寒冷暴露)使 MSNA 的增加明显小于腺苷。此外,臂内茶碱(每分钟 1 μg/ml 前臂)的腺苷受体拮抗作用阻断了输注中等长握力(最大自主收缩的 30%)产生的 MSNA(92+/-15% vs. 28+/-6%,n = 7,P < 0.01)和 MABP(38+/-6 vs. 27+/-4 mmHg,P = 0.01)的增加。手臂,但不是对侧手臂。茶碱并不能阻止握力引起的心率增加,这种反应更多地由中枢命令介导,而不是肌肉传入激活。我们认为内源性腺苷有助于激活参与人类运动按压反射的肌肉传入神经。
Isometric exercise increases sympathetic nerve activity and blood pressure. This exercise presser reflex is partly mediated by metabolic products activating muscle afferents (metaboreceptors). Whereas adenosine is a known inhibitory neuromodulater, there is increasing evidence that it activates afferent nerves. We, therefore, examined the hypothesis that adenosine stimulates muscle afferents and participates in the exercise presser reflex in healthy volunteers. Intraarterial administration of adenosine into the forearm, during venous occlusion to prevent systemic effects, mimicked the response to exercise, increasing muscle sympathetic nerve activity (MSNA, lower limb microneurography) and mean arterial blood pressure (MABP) at all doses studied (2, 3, and 4 mg). Heart rate increased only with the highest dose. Intrabrachial adenosine (4 mg) increased MSNA by 96+/-25% (n = 6, P < 0.01)and MABP by 12+/-3 mmHg (P < 0.01). Adenosine produced forearm discomfort, but equivalent painful stimuli (forearm ischemia and cold exposure) increased MSNA significantly less than adenosine. Furthermore, adenosine receptor antagonism with intrabrachial theophylline (1 mu g/ml forearm per min) blocked the increase in MSNA (92+/-15% vs. 28+/-6%, n = 7, P < 0.01) and MABP (38+/-6 vs. 27+/-4 mmHg, P = 0.01) produced by isometric handgrip (30% of maximal voluntary contraction) in the infused arm, but not the contralateral arm. Theophylline did not prevent the increase in heart rate produced by handgrip, a response mediated more by central command than muscle afferent activation. We propose that endogenous adenosine contributes to the activation of muscle afferents involved in the exercise presser reflex in humans.