英国学者最近以大鼠进行实验后推断,引发高血压的祸首,可能是脑部血管的一种蛋白质,医界可望据此为高血压治疗另寻疗法。
这篇研究将刊载于最新一期的Hypertension中,高血压是现代人健康的杀手,占病例绝大部份的「原发性高血压」却找不出特定致病原因,医师通常只能针对症状给予治疗。
英国布里斯托大学Julian Paton教授领导的团队,以大鼠为实验动物,在脑部血管壁找到一种「连接黏附分子一型蛋白质」(JAM-1),发现它会吸引白血球,造成血管壁发炎,阻碍血液流动,降低脑部氧气供应,导致血压升高。
研究人员表示,相关的作用机转还不清楚,但JAM-1蛋白质可为治疗高血压提供新线索。未来,科学家们将进一步厘清脑部血管的发炎型态,然后对症下药。
编按:据统计,英国民众约有三分之一有高血压症状,全世界高血压人口更多达六亿人。台湾地区高血压盛行率,十五岁以上男性24.9%,女性18.2%。高血压初期症状并不明显,若未妥善治疗,很容易导致中风、冠状动脉心脏病、心脏衰竭、心肌梗塞、肾脏病变等严重疾病。
(资料来源 : Bio.com)
英文原文链接:
http://www.bio.com/newsfeatures/newsfeatures_research.jhtml?cid=28300006
原始出处:
Published online before print April 9, 2007
(Hypertension 2007, doi:10.1161/HYPERTENSIONAHA.106.085589)
Junctional Adhesion Molecule-1 Is Upregulated in Spontaneously Hypertensive Rats. Evidence for a Prohypertensive Role Within the Brain Stem
Hidefumi Waki*; Beihui Liu; Masao Miyake; Kiyoaki Katahira; David Murphy; Sergey Kasparov; and Julian F.R. Paton
From the Department of Physiology, Bristol Heart Institute, School of Medical Sciences (H.W., B.L., S.K., J.F.R.P.), and Henry Wellcome Laboratories for Integrated Neuroscience and Endocrinology (D.M.), University of Bristol, Bristol, United Kingdom; and the Department of Physiology (M.M.) and Experimental Animal Center (K.K.), Fukushima Medical University School of Medicine, Fukushima, Japan
* To whom correspondence should be addressed. E-mail: h-waki@wakayama-med.ac.jp .
Abstract--Junctional adhesion molecule-1 (JAM-1) forms part of the tight junction between adjacent endothelial cells. Using microarray technology, we showed previously that JAM-1 was differentially expressed in the brain stem of spontaneously hypertensive rats compared with normotensive Wistar-Kyoto (WKY) rats. In this study, we quantified the expression of JAM-1 in the brain stem of spontaneously hypertensive rats and WKY rats and established whether any differential expression was confined to this region of the brain or was ubiquitous throughout the central nervous system and, indeed, the whole body. Because the nucleus tractus solitarii plays a pivotal role in arterial pressure regulation, we assessed whether JAM-1 in this region affects the chronic regulation of arterial pressure. Real time RT-PCR revealed that JAM-1 mRNA was upregulated in multiple regions of the brain and all of the peripheral vascular beds studied. In the nucleus tractus solitarii, the level of JAM-1 mRNA was significantly higher in both young (3-week-old, prehypertensive) and adult male spontaneously hypertensive rats (15 to 18 weeks old) than that of age-matched WKY rats (fold differences; prehypertensives: 1.01±0.06 versus 1.59±0.13; n=10; P<0.01; adult: 1.08±0.14 versus 2.86±0.57; n=10; P<0.01). After adenoviral-mediated expression of JAM-1 in the nucleus tractus solitarii of adult WKY rats (15 weeks old; n=6), systolic pressure was increased from 120±4 to 132±4 mm Hg (P<0.01). Our data suggest that JAM-1 expression in the spontaneously hypertensive rat is upregulated throughout the body compared with the WKY rat and that this is not secondary to the hypertension. When JAM-1 is expressed in the nucleus tractus solitarii, it raises arterial pressure, suggesting a novel prohypertensive role for this protein within the brain stem.
Key words: hypertension • brain stem • inflammation • baroreflex control • adhesion molecules