Matsukawa K, Sadamoto T, Tsuchimochi H, Komine H, Murata J, Shimizu K
Department of Physiology, Institute of Health Sciences, Hiroshima University Faculty of Medicine, Hiroshima, 734-8551 Japan.
Jpn J Physiol. 2001 Oct;51(5):591-7. doi: 10.2170/jjphysiol.51.591.
To examine a hypothesis of whether static muscle contraction produces a release of catecholamines from the adrenal medulla via reflex stimulation of preganglionic adrenal sympathetic nerve activity induced by receptors in the contracting muscle, we compared the reflex responses in a concentration of epinephrine (Ep) and norepinephrine (NEp) in arterial plasma during static contraction and during a mechanical stretch of the hindlimb triceps surae muscle in anesthetized cats. Static contraction was evoked by electrically stimulating the peripheral ends of the cut L(7) and S(1) ventral roots at 20 or 40 Hz. Mean arterial pressure (MAP) and heart rate (HR) increased 23 +/- 3.1 mmHg and 19 +/- 4.3 beats/min during static contraction. Ep in arterial plasma increased 0.18 +/- 0.072 ng/ml over the control of 0.14 +/- 0.051 ng/ml within 1 min from the onset of static contraction, and NEp increased 0.47 +/- 0.087 ng/ml over the control of 0.71 +/- 0.108 ng/ml. Following a neuromuscular blockade, although the same ventral root stimulation failed to produce the cardiovascular and plasma catecholamine responses, the mechanical stretch of the muscle increased MAP, HR, and plasma Ep, but not plasma NEp. With bilateral adrenalectomy, the baseline Ep became negligible (0.012 +/- 0.001 ng/ml) and the baseline NEp was lowered to 0.52 +/- 0.109 ng/ml. Neither static contraction nor mechanical stretch produced significant responses in plasma Ep and NEp following the adrenalectomy. These results suggest that static muscle contraction augments preganglionic adrenal sympathetic nerve activity, which in turn secretes epinephrine from the adrenal medulla into plasma. A muscle mechanoreflex from the contracting muscle may play a role in stimulation of the adrenal sympathetic nerve activity.
为检验如下假说,即静态肌肉收缩是否通过收缩肌肉中的受体诱导节前肾上腺交感神经活动的反射性刺激,从而促使肾上腺髓质释放儿茶酚胺,我们比较了麻醉猫后肢腓肠肌在静态收缩和机械拉伸过程中动脉血浆中肾上腺素(Ep)和去甲肾上腺素(NEp)浓度的反射反应。通过以20或40赫兹电刺激切断的L(7)和S(1)腹根外周端诱发静态收缩。静态收缩期间,平均动脉压(MAP)和心率(HR)分别升高23±3.1 mmHg和19±4.3次/分钟。静态收缩开始后1分钟内,动脉血浆中的Ep在对照值0.14±0.051 ng/ml的基础上增加了0.18±0.072 ng/ml,NEp在对照值0.71±0.108 ng/ml的基础上增加了0.47±0.087 ng/ml。神经肌肉阻滞之后,尽管相同的腹根刺激未能产生心血管和血浆儿茶酚胺反应,但肌肉的机械拉伸增加了MAP、HR和血浆Ep,但未增加血浆NEp。双侧肾上腺切除术后,基线Ep变得微不足道(0.012±0.001 ng/ml),基线NEp降至0.52±0.109 ng/ml。肾上腺切除术后,静态收缩和机械拉伸均未在血浆Ep和NEp中产生显著反应。这些结果表明,静态肌肉收缩增强了节前肾上腺交感神经活动,进而促使肾上腺素从肾上腺髓质分泌到血浆中。来自收缩肌肉的肌肉机械反射可能在刺激肾上腺交感神经活动中起作用。