Leptin signaling in the nucleus of the solitary tract alters the cardiovascular responses to activation of the chemoreceptor reflex
Leptin signaling in the nucleus of the solitary tract alters the cardiovascular responses to activation of the chemoreceptor reflex
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DOI：
10.1152/ajpregu.00068.2012
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发表时间：
2012-10-01
影响因子：
2.8
通讯作者：
Moreau, Jason M.
中科院分区：
文献类型：
--
作者：
Ciriello, John;Moreau, Jason M.
作者声明：John J.孤束核中的瘦素信号改变化学感受器反射激活的心血管反应。Am J Physiol Regul Integr Comp Physiol 303：R727-R736，2012年。首次发表于2012年8月22日; doi：10.1152/ajpregu.00068.2012.-在患有慢性间歇性缺氧（CIH）的个体中，瘦素的循环水平升高。全身和中枢给予瘦素可增强交感神经活动（SNA）、动脉压（AP）和心率（HR），并减弱压力感受器反射，这是与CIH期间观察到的由于全身缺氧激活化学感受器而引起的心血管反应相似的反应。因此，本实验在麻醉Wistar大鼠上研究孤束核（NTS）内瘦素对NTS神经元激活过程中的AP、HR反应和肾SNA（RSNA）反应以及化学感受器反射的影响。将瘦素（5-100 ng; 20 nl）微量注射到尾侧NTS升压部位（L-谷氨酸; L-Glu; 0.25 M; 10 nl）引起AP、HR和RSNA的剂量相关性增加。向这些部位微量注射瘦素（5 ng; 20 nl）可增强L-Glu引起的AP和HR增加。此外，双侧注射瘦素（5 ng; 100 nl）到NTS增强AP的增加和衰减的心动过缓的化学反射的全身激活。在Zucker肥胖大鼠中，将瘦素注射到NTS中既不引起心血管反应，也不改变对化学反射激活的心血管反应。两者合计，这些数据表明，瘦素发挥调节作用的NTS内的神经元回路，控制心血管反应引起的动脉化学感受器的反射激活过程中，并建议增加AP和SNA观察到的CIH的个人可能是由于，在一定程度上，瘦素的影响，在NTS的水平上的化学反射。
Ciriello J, Moreau JM. Leptin signaling in the nucleus of the solitary tract alters the cardiovascular responses to activation of the chemoreceptor reflex. Am J Physiol Regul Integr Comp Physiol 303: R727-R736, 2012. First published August 22, 2012; doi:10.1152/ajpregu.00068.2012.-Circulating levels of leptin are elevated in individuals suffering from chronic intermittent hypoxia (CIH). Systemic and central administration of leptin elicits increases in sympathetic nervous activity (SNA), arterial pressure (AP), and heart rate (HR), and it attenuates the baroreceptor reflex, cardiovascular responses that are similar to those observed during CIH as a result of activation of chemoreceptors by the systemic hypoxia. Therefore, experiments were done in anesthetized Wistar rats to investigate the effects of leptin in nucleus of the solitary tract (NTS) on AP and HR responses, and renal SNA (RSNA) responses during activation of NTS neurons and the chemoreceptor reflex. Microinjection of leptin (5-100 ng; 20 nl) into caudal NTS pressor sites (L-glutamate; L-Glu; 0.25 M; 10 nl) elicited dose-related increases in AP, HR, and RSNA. Leptin microinjections (5 ng; 20 nl) into these sites potentiated the increase in AP and HR elicited by L-Glu. Additionally, bilateral injections of leptin (5 ng; 100 nl) into NTS potentiated the increase in AP and attenuated the bradycardia to systemic activation of the chemoreflex. In the Zucker obese rat, leptin injections into NTS neither elicited cardiovascular responses nor altered the cardiovascular responses to activation of the chemoreflex. Taken together, these data indicate that leptin exerts a modulatory effect on neuronal circuits within NTS that control cardiovascular responses elicited during the reflex activation of arterial chemoreceptors and suggest that increased AP and SNA observed in individuals with CIH may be due, in part, by leptin's effects on the chemoreflex at the level of NTS.