经济学人 第五集 Hypertension
Hypertension
Raising possibilities
Apr 19th 2007
From The Economist print edition
高血压：大脑可能性增加
High blood pressure may originate in the brain
高血压可能源于大脑
THE first step to defeating an enemy is to pin down his exact identity and how he operates.
Hypertension—chronic, abnormally raised blood pressure—causes heart attacks, strokes and a multitude of other nasty conditions. Around a third of Americans and Britons suffer from it. It is thus a worthy enemy and nailing its cause is a priority. Until now, this has mostly seemed to lie in the kidneys. But Hidefumi Waki and Julian Paton of Bristol University think they have gathered some valuable new intelligence—by studying the brain.
打败敌人首先要了解其身份，以及其运作方式。高血压是血压反常、慢性地升高，这会导致心脏病、中风和其它的多种危险疾病。大约三分之一的英美人患有高血压。因此，高血压是一个劲敌，我们首先要找到其根源。直到现在，大多数人认为根源在于肾。但是，Bristol大学的Hidefumi Waki和Julian Paton通过对大脑的研究，认为他们收集了一些有价值的新信息。
In a previous experiment Dr Waki and Dr Paton had found that rodents with high blood pressure expressed some genes differently in an area of the brain, called the solitary nucleus, which sets the body's normal blood-pressure level. One of these genes was called “junctional adhesion molecule-1” or JAM-1 for short. It is a molecule normally found in the walls of blood vessels that attracts clotting and immune cells—in other words, it causes inflammation. So the pair decided to look at JAM-1 in further depth.
Waki和Paton博士在前一次实验中发现，啮齿动物患上高血压后，它们大脑中一个称为孤束核的部位具有不同的基因表达，这个部位是负责把身体调整到正常的血压水平的。其中一个基因是“接合粘附分子1号（Junctional Adhesion Molecule-1）”，简称为JAM-1。该分子通常存在于吸引凝血细胞和免疫细胞的血管壁，也就是说，它会导致炎症。因此，两人决定更深入地研究JAM-1分子。
They found that in rats with high blood pressure JAM-1 levels were raised not only in the brain but also the kidney, spleen, lungs and skeletal muscle. To find out whether this was the cause or effect of high blood pressure, they then transferred the JAM-1 gene into the solitary nucleus of normal rats. After two weeks, these rats suffered from higher blood pressure than rats that had not received the gene. The researchers will publish the work next month in Hypertension.
Waki和Paton博士发现，老鼠患上高血压后，不仅大脑的JAM-1水平，而且肾、脾、肺和骨骼肌的JAM-1水平都升高了。为了查出这是否是高血压的根源，以及高血压的影响，两人把JAM-1转移到正常老鼠的孤束核中。两星期后，这些老鼠的血压比没有接受JAM-1基因的老鼠的血压高。相关工作会在下个月的《高血压》杂志中发表。
Previously, experts thought that high blood pressure was caused by the kidneys. The idea was that the kidneys failed to sense the blood pressure. This then caused the lungs to make a hormone that increases blood pressure, leading to a chain of events that raised pressure throughout the blood-vessel network. All blood-pressure-lowering drugs work by seeking to put this right. Yet blaming the kidneys cannot be the full explanation of what is going on, because only half the sufferers respond to blood-pressure-lowering drugs.
以前，专家们认为高血压是由肾引起的。因为肾对血压的感应功能失效使肺分泌一种荷尔蒙来升高血压，这会引起一连串事件，增加血管网络的压力。所有降压药都是为了使血压感应功能恢复正常。但是，把根源归于肾并不能解释所有发生的事实，因为降压药只对一半的病人有效。
Uncovering exactly how raised levels of JAM-1 disrupt the brain's ability to control blood pressure is the next step in tackling the disease. Dr Paton predicts that the molecule may alter levels of neurotransmitters, which control how signals pass from one nerve to the next. Perhaps, peripheral blood vessels are mistakenly told to constrict, increasing blood pressure.
JAM-1分子水平的升高是如何破坏大脑控制血压的能力的呢？战胜高血压的下一步就是要正确地解决这个问题。Paton博士预测，JAM-1分子可能改变了神经递质水平，而神经递质负责控制神经间的信号传递。或许，外围血管被错误地告知，需要其压缩，从而使血压升高。
Although these findings are preliminary, they have far-reaching implications. Variations in the JAM-1 gene and its expression may explain why high blood pressure tends to run in families, although it is also caused by a poor diet. The finding also shows that the brain could increase the activity of the sympathetic nerves, the part of the nervous system involved in stress response. Ultimately, the finding could hasten the development of drugs that would attack hypertension at its source, stopping its deadly consequences in their tracks.
这只是初步的发现，却具有深远的含义。虽然缺乏饮食也会导致高血压，JAM-1基因及其表达的差异也可以解释高血压会在家族成员中流传的原因。这些发现也显示，大脑能增加交感神经的活动，而交感神经是负责压力响应的神经系统。最后，这些发现会加速药品的开发，从根源上战胜高血压，阻止灾难性后果的发生。
