Paton Julian F R, Waki Hidefumi, Abdala Ana P L, Dickinson John, Kasparov Sergey
Department of Physiology, Bristol Heart Institute, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, UK.
Curr Hypertens Rep. 2007 Jun;9(3):242-7. doi: 10.1007/s11906-007-0043-1.
Paracrine signaling by nitric oxide (NO) released from microvasculature within the brain affects multiple neuronal functions. Reviewed here is a role in central cardiovascular control. Within the nucleus tractus solitarii (NTS), a major regulatory region for arterial pressure, angiotensin II stimulates NO generation from endothelial nitric oxide synthase (eNOS). This enhances c-aminobutyric acid release to depress baroreflex function. In the spontaneously hypertensive rat (SHR), eNOS mRNA in the NTS is elevated compared to normotensive rats. Chronic inhibition of eNOS activity in the NTS of SHR reduced arterial pressure and increased baroreflex gain. Thus, eNOS-generated NO in the NTS plays a major role in control of baroreflex gain and arterial pressure. Indeed, its activity contributes to hypertension in the SHR. We propose that eNOS-generated NO in the SHR may be a compensatory mechanism for any potential threat to an adequate blood supply to the brain (eg, from genetically small arteries supplying the brainstem).
从脑内微脉管系统释放的一氧化氮（NO）通过旁分泌信号传导影响多种神经元功能。本文综述其在中枢心血管控制中的作用。在孤束核（NTS）这个主要的动脉血压调节区域内，血管紧张素II刺激内皮型一氧化氮合酶（eNOS）产生NO。这会增强γ-氨基丁酸的释放，从而抑制压力反射功能。与正常血压大鼠相比，自发性高血压大鼠（SHR）的NTS中eNOS mRNA水平升高。对SHR的NTS中eNOS活性进行长期抑制可降低动脉血压并增加压力反射增益。因此，NTS中由eNOS产生的NO在压力反射增益和动脉血压的控制中起主要作用。实际上，其活性促成了SHR的高血压。我们提出，SHR中由eNOS产生的NO可能是对脑充足血液供应的任何潜在威胁（例如，来自供应脑干的遗传性小动脉）的一种代偿机制。
