Central oxytocin modulates exercise-induced tachycardia
Central oxytocin modulates exercise-induced tachycardia
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DOI：
10.1152/ajpregu.2000.278.6.r1474
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发表时间：
2000-06-01
影响因子：
2.8
通讯作者：
Michelini, LC
中科院分区：
文献类型：
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作者：
Braga, DC;Mori, E;Michelini, LC
我们已经证明，在运动期间，运动大鼠(T)和久坐大鼠(S)的抗利尿激素向脑干背侧的传导被激活，并促进运动性心动过速（Dufloth DL， Morris M和Michelini LC）。[J] .中国生物医学工程学报，2009(5):444 - 444。在本研究中，我们研究了催产素对孤立束核（NTS）和迷走神经背运动核（DMV）复合体（NTS/DMV）的投射是否参与了T和S大鼠对运动的差异心率（HR）反应。在NTS/DMV中分别用载药（生理盐水）、催产素（OT; 20 pmol/200 nl）或OT受体拮抗剂（OTant; 20 pmol/200 nl）预处理S和T，比较动态运动（0.4-1.4 km/h）时的动脉压（AP）和HR反应。在不同的S组和T组中，分别在休息时和运动后立即测量特定脑区和血浆中的OT含量。运动只增加了T大鼠脑干背侧（4.5倍）、脑干腹侧（2.7倍）和脊髓（3.4倍）的OT含量。T大鼠的神经分泌区、内侧隆起和垂体后叶未见明显变化，但运动后血浆水平立即降低。阻断NTS/DMV OT受体不会改变基础平均AP （MAP）和HR或MAP对运动的反应。然而，OTant仅在T组增强运动诱发的心动过速（平均增加26%）。在NTS/DMV中使用外源性OT预处理可以减弱S和T大鼠的心动过速反应，但不会改变MAP反应。给药OT受体拮抗剂或OT进入第四脑室对动态运动的心血管反应没有影响。综上所述，结果表明，当T大鼠运动时，NTS/DMV的催产素投射受到刺激，并且在此水平上释放的OT作用于OT受体以抑制运动诱导的心动过速。
We have shown that vasopressinergic projections to dorsal brain stem are activated during exercise and facilitate exercise tachycardia in both trained (T) and sedentary (S) rats (Dufloth DL, Morris M, and Michelini LC. Am J Physiol Regulatory Integrative Comp Physiol 273: R1271-R1282, 1997). In the present study, we investigated whether oxytocinergic projections to the nucleus of the solitary tract (NTS) dorsal motor nucleus of the vagus (DMV) complex (NTS/DMV) are involved in the differential heart rate (HR) response to exercise in T and S rats. Arterial pressure (AP) and HR responses to dynamic exercise (0.4-1.4 km/h) were compared in S and T pretreated with vehicle (saline), oxytocin (OT; 20 pmol/200 nl) or OT-receptor antagonist (OTant; 20 pmol/200 nl) into the NTS/DMV. OT content in specific brain regions and plasma were measured in separate S and T groups at rest and immediately after exercise. Exercise increased OT content in dorsal (4.5-fold) and ventral brain stem (2.7-fold) and spinal cord (3.4-fold) only in T rats. No significant changes were observed in neurosecretory regions or medial eminence and posterior pituitary, but plasma levels of T rats were reduced immediately after exercise. Blockade of NTS/DMV OT receptors did not change basal mean AP (MAP) and HR or the MAP response to exercise. However, OTant potentiated exercise-induced tachycardia (average increase of 26%) only in the T group. Pretreatment with exogenous OT in the NTS/DMV blunted the tachycardic response both in S and T rats without changing the MAP response. Administration of OT-receptor antagonist or OT into the fourth cerebral ventricle had no effect on the cardiovascular response to dynamic exercise. Taken together, the results suggest that oxytocinergic projections to the NTS/DMV are stimulated when T rats exercise and that OT released at this level acts on OT receptors to restrain exercise-induced tachycardia.