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内皮─氧化氮的减少引起Dahl高血压大鼠异常的血管反应
作者单位:天津南开医院!300100(丁洁,吴咸中),日本香川医科大学(西田育弘)
摘    要:本文研究目的在于观察Dahl高血压大鼠对去甲肾上腺素(NE)收缩反应增强,对乙酰胆碱(ACH)舒张反应减弱,是否与血管内皮NitricOxide(NO)有关。7—8周龄雄性Dahl盐敏感(DS)大鼠和盐抵抗(DR)大鼠,各随机分两组,分别给予正常盐或高盐饮食,每周尾套管法测血压和体重,4周后麻醉状态下取胸主动脉,用于离体血管反应性研究。结果显示:高盐饮食的DS大鼠尾动脉血压明显升高,NE诱导的收缩反应也明显高于其它三组,去内皮及体外L—NAME的处理,可以消除这一差别。同时Dahl高血压大鼠,ACh诱导的舒张反应也明显减弱。体外Larginine的使用,不同程度地降低了NE诱导的收缩反应,但不能废除组间差异。结论:NO合成酶功能障碍可能是Dahl高血压大鼠异常血管反应的原因。

关 键 词:一氧化氮  离体血管反应  Dahl鼠

DECREASED NITRIC OXIDE IS RESPONSIBLE FOR THE ABNORMAL VASCULAR RESPONSES TO NE AND ACh IN HYPERTENSIVE DAHL RAT
Authors:Ding Jie  Wu Jingzhong  
Institution:Tianjin Nankai Hospital. Tianjn 300100
Abstract:The study was intended to investigate Whether an enhanced constriction response to norepinephrine (NE) and a reduced en-dothelium - dependent relaxing response to acetylcholine (ACh) was relevant to the hy-pertensive Dahl rats or not. The 7-8weeks old male Dahl salt-sensitive (DS) and salt - resistant (DR) rats were partly fed by normal salt diet (0. 4%NaCL) or partly fed by high salt diet (8%NaCL). The aortic rings with or without endothelium were used to investigate the vascular responses to NE and ACh. Systolic blood pressure was elevated significantly (P<0.05) in the DS rats fed by 8%NaCL but not in the DS rats fed by 0. 4% NaCL and the DR rats fed by either 8% or 0. 4% NaCL, In the hyperten-sive Dahl rast, NE - induced constricting response was significantly higher, Remove of endothelium and L - NAME treatment abrogated the differences between the groups. Endothelium - dependent relax-ation to ACh, in the hypertensive Dahl rats, exhibited markedly lower than the other three groups. L-arginine treatment in vit-ro did not dispel the differences of NE -in- duced responses between the hypertensive Dahl rats and the nomotensive Dahl rats. Our data suggested that impaired L - arginine NO pathway should be responsible for the abnormal vascular responses to NE and ACh. Dysfunction of NO production is likeiy due to redueced activation of NOS.
Keywords:Nitris Oxide Dahl rats Isolated vascular responses
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