Leptin into the rostral ventral lateral medulla (RVLM) augments renal sympathetic nerve activity and blood pressure.

Leptin into the rostral ventral lateral medulla (RVLM) augments renal sympathetic nerve activity and blood pressure.
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瘦素进入腹侧腹侧髓质(RVLM)增强肾交感神经活性和血压。

DOI:
10.3389/fnins.2014.00232
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发表时间:
2014
影响因子:
4.3
通讯作者:
McDougal DH
McDougal DH
中科院分区:
医学2区
文献类型:
--
作者:
Barnes MJ;McDougal DH

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瘦素是一种从脂肪组织释放的激素。虽然这种激素通常会减少进食行为并增加能量消耗,但在肥胖症中,即使激素大量释放,对这些作用也会产生抵抗力。虽然瘦素不再抑制肥胖者的进食,但瘦素对其他自主功能(如血压调节)仍有强大的作用。瘦素与高血压和交感神经自主活动增加有关。因此,瘦素正在成为肥胖中观察到的高血压状态的主要贡献者。交感神经对血压的控制主要是通过脑干尾部的自主反射控制回路来维持的。延髓头端腹外侧区(RVLM)是交感神经系统的主要调节器,将兴奋性纤维发送到交感节前神经元以调节交感神经对阻力血管和血压的控制。本实验室先前的研究表明,延髓腹外侧区的神经元表达瘦素受体(ObRb)。我们目前的研究使用假狂犬病多突触逆行追踪和免疫组化方法显示,RVLM内的神经元,发送交感神经投射到肾脏表达瘦素受体。RVLM内急性微量注射瘦素(1和3 μg; 40 nL)引起平均动脉压(MAP)和肾交感神经活动(RSNA)显著增加。当在3 μg剂量的瘦素之前用瘦素拮抗剂(SLAN-4; 1 ng)时,其减弱瘦素的心血管反应。总之,这些数据表明,瘦素的RVLM内的行动可能会影响血压和肾交感神经活动。
Leptin is a hormone released from adipose tissue. While this hormone normally acts to reduce feeding behavior and increase energy expenditure, in obesity, resistance to these effects occurs even though the hormone is released in large amounts. Although leptin no longer works to suppress feeding in the obese, leptin retains its potent effects on other autonomic functions such as blood pressure regulation. Leptin has been associated with hypertension and increased sympathetic autonomic activity. Therefore, leptin is emerging as a major contributor to the hypertensive state observed in obesity. Sympathetic control of blood pressure is maintained principally by autonomic reflex control circuits in the caudal brainstem. The rostral ventral-lateral medulla (RVLM) is the primary regulator of the sympathetic nervous system, sending excitatory fibers to sympathetic preganglionic neurons to regulate sympathetic control over resistance vessels and blood pressure. Previous studies from our laboratory have shown that neurons in the ventral lateral medulla express leptin receptors (ObRb). Our present study using pseudo-rabies multi-synaptic retrograde tract tracing and immunohistochemical methods revealed that neurons within the RVLM that send sympathetic projections to the kidney express leptin receptors. Acute microinjection of leptin (1 and 3 μg; 40 nL) into the RVLM evoked a significant increase in Mean Arterial Pressure (MAP) and renal sympathetic nerve activity (RSNA). When the 3 μg dose of leptin was preceded with a leptin antagonist, (SLAN-4; 1 ng), it attenuated the cardiovascular response of leptin. Taken together, these data suggest that leptin's actions within the RVLM may influence blood pressure and renal sympathetic nerve activity.
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