摘要
目的观察慢性盐负荷对AngⅡ模型大鼠血压及血管平滑肌钙激活性氯通道(mCLCA4)表达的影响。方法选取12周龄SD大鼠随机分为AngⅡ模型组和对照组。模型组用AngⅡ药泵(100ng·kg-1·min-1)皮下输注2周;对照组除不给予AngⅡ干预外与模型组相同,正常饲养2周。2周后去除模型组药泵,于2组中各选6只取材分析后,再将模型组和对照组各分为高盐组(4%NaCl)和正常盐组(0.6%NaCl)干预12周。观察大鼠的钠代谢及血压变化。自盐负荷起,每隔4周取材用标记好的寡核苷酸探针通过原位杂交观察各组大鼠动脉血管平滑肌钙激活性氯通道mCLCA4mRNA的表达变化。结果输注AngⅡ2周的模型组大鼠较对照组血压明显升高(P<0.05),但血管平滑肌mCLCA4mRNA的表达在两组间无明显差别。模型大鼠的高盐组与正常盐组在各时点的血压均无明显差异;高盐干预4周时,血管平滑肌mCLCA4mRNA的表达在两组间无显著差别;高盐干预至8周及12周时,高盐组mCLCA4mRNA的表达明显高于同时点正常盐组(P<0.01)。对照组中,高盐组各时点血管平滑肌mCLCA4的表达水平均比正常盐组明显升高(P<0.05),但两组间各时点血压并无明显差异。结论给SD大鼠AngⅡ(100ng·kg-1·min-1)皮下慢性输注,可使其血压升高,但AngⅡ引起血压升高的机制可能和mCLCA4的表达变化无直接联系。AngⅡ输注2周可对抗短期高盐干预(4周)使mCLCA4mRNA表达上调的作用。高盐摄入对正常SD大鼠血管平滑肌mCLCA4mRNA的表达有上调作用,但对其血压无显著升压作用,说明mCLCA4的表达上调可能拮抗盐的升压作用。
Objective To investigate the effects of salt loading on blood pressure and the expression of arterial chloride channel in rats with elevated blood pressure induced by angiotensin Ⅱ （AngⅡ）. Methods Male 12-week-old SD rats were randomly divided into AngⅡ and control groups, and in the former group, the rats were exposed to subcutaneous AngⅡ infusion delivered via a drug pump （at 100 ng ·kg^-1 ·min^-1） for 2 weeks. After the exposure, each group of the rats was further divided into 2 subgroups to receive a high-salt diet （4% NaCl） or normal salt diet （0.6% NaCl） for 12 weeks. The tail blood pressure and sodium metabolism of the rats were measured during the experiment. Since the commencement of salt loading, 6 rats were sacrificed every 4 weeks to obtain the artery samples, in which mCLCA4 mRNA expression in the arterial smooth muscles was detected by in situ hybridization using mCLCA4 oligonuclear probe. Results The blood pressure of rats in Ang Ⅱ group was significantly higher than that of the control rats （P〈0.05）, but Ang Ⅱ did not produce significant effects on the expression of mCLCA4, mCLCA4 mRNA expression was significantly increased in the arterial smooth muscle cells of the rats in high salt groups as compared with those in normal salt groups （P〈0.05）. Conclusions A sub-pressor dose of AngII can result in blood pressure elevation, but the mechanism of which does not seem to involve mCLCA4 expression, mCLCA4 mRNA expression is up-regulated in normal SD rats after high salt feeding, but salt loading does not obviously affect blood pressure, suggesting the role ofmCLCA4 in antagonizing the pressure-elevating effect of salt loading.
出处
《南方医科大学学报》
CAS
CSCD
北大核心
2008年第1期7-11,共5页
Journal of Southern Medical University
基金
美中医学基金(CMB)资助(#01-761)~~
关键词
钙激活性氯通道
AngⅡ
盐负荷
高血压
calcium activated chloride channel
angiotensin Ⅱ
salt loading
hypertension
