Circulating angiotensin II and dietary salt: Converging signals for neurogenic hypertension
Circulating angiotensin II and dietary salt: Converging signals for neurogenic hypertension
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DOI：
10.1007/s11906-007-0041-3
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发表时间：
2007-06-01
影响因子：
5.6
通讯作者：
Raizada, Moban K.
中科院分区：
文献类型：
--
作者：
Osborn, Jobn W.;Fink, Gregory D.;Raizada, Moban K.
循环血管紧张素II（Ang II）与高盐摄入相结合，增加了某些形式的高血压的交感神经活动（SNA）。血管紧张素II诱导的SNA增加是适度的，延迟的，特定于某些血管床。循环血管紧张素II的脑靶点是最后区（AP）、穹窿下器官（SFO）和可能的其他脑室周围器官中的神经元。Ang II信号传导与SFO和/或终板血管器（OVLT）中的钠敏感神经元整合，并通过室旁核（PVN）驱动延髓头端腹外侧（RVLM）中的交感运动前神经元。很可能，随着时间的推移，新的基因表达模式出现在SFO-PVN-RVLM通路的神经元内，改变了它们的信号传导特性。这一转变对维持国民账户体系的增长至关重要。支持这一过程的新基因的鉴定可能为神经源性高血压的治疗提供新的靶点。
Circulating angiotensin II (Ang II) combined with high salt intake increases sympathetic nerve activity (SNA) in some forms of hypertension. Ang II-induced increases in SNA are modest, delayed, and specific to certain vascular beds. The brain targets for circulating Ang II are neurons in the area postrema (AP), subfornical organ (SFO), and possibly other circumventricular organs. Ang II signaling is integrated with sodium-sensitive neurons in the SFO and/or organum vasculosum of the lamina terminalis (OVLT) and drives sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM) via the paraventricular nucleus (PVN). It is likely that, over time, new patterns of gene expression emerge within neurons of the SFO-PVN-RVLM pathway that transform their signaling properties. This transformation is critical in maintaining increased SNA. Identification of a novel gene supporting this process may provide new targets for treatment of neurogenic hypertension.