英國(guó)學(xué)者最近以大鼠進(jìn)行實(shí)驗(yàn)后推斷,，引發(fā)高血壓的禍?zhǔn)?，可能是腦部血管的一種蛋白質(zhì)，醫(yī)界可望據(jù)此為高血壓治療另尋療法,。
這篇研究將刊載于最新一期的Hypertension中,，高血壓是現(xiàn)代人健康的殺手，占病例絕大部份的「原發(fā)性高血壓」卻找不出特定致病原因,，醫(yī)師通常只能針對(duì)癥狀給予治療,。
英國(guó)布里斯托大學(xué)Julian Paton教授領(lǐng)導(dǎo)的團(tuán)隊(duì),，以大鼠為實(shí)驗(yàn)動(dòng)物,，在腦部血管壁找到一種「連接黏附分子一型蛋白質(zhì)」（JAM-1）,，發(fā)現(xiàn)它會(huì)吸引白血球,，造成血管壁發(fā)炎，阻礙血液流動(dòng),，降低腦部氧氣供應(yīng)，導(dǎo)致血壓升高,。
研究人員表示,，相關(guān)的作用機(jī)轉(zhuǎn)還不清楚,，但JAM-1蛋白質(zhì)可為治療高血壓提供新線索,。未來，科學(xué)家們將進(jìn)一步厘清腦部血管的發(fā)炎型態(tài),，然后對(duì)癥下藥,。
編按：據(jù)統(tǒng)計(jì)，英國(guó)民眾約有三分之一有高血壓癥狀，全世界高血壓人口更多達(dá)六億人,。臺(tái)灣地區(qū)高血壓盛行率，十五歲以上男性24.9％,，女性18.2％。高血壓初期癥狀并不明顯,，若未妥善治療,，很容易導(dǎo)致中風(fēng),、冠狀動(dòng)脈心臟病,、心臟衰竭、心肌梗塞,、腎臟病變等嚴(yán)重疾病。
(資料來源 : Bio.com)
英文原文鏈接：
http://www.bio.com/newsfeatures/newsfeatures_research.jhtml?cid=28300006
原始出處:
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: [email protected] .
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
