Referenced in: none

Automatically associated channels: ClC4 , ClCA4

Title: [Effects of chronic salt loading on blood pressure and arterial chloride channel expression in rats with a two-week-long angiotensin II exposure]

Authors: Yuan Fang, Zhi-Quan Liu, Yong Zheng

Journal, date & volume: Nan Fang Yi Ke Da Xue Xue Bao, 2008 Jan , 28, 7-11

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/18227015

Abstract
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).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 mCLCA(4) mRNA expression in the arterial smooth muscles was detected by in situ hybridization using mCLCA(4) oligonuclear probe.The blood pressure of rats in AngII group was significantly higher than that of the control rats (P<0.05), but AngII did not produce significant effects on the expression of mCLCA(4). 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).A sub-pressor dose of AngII can result in blood pressure elevation, but the mechanism of which does not seem to involve mCLCA(4) expression. mCLCA(4) 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 of mCLCA(4) in antagonizing the pressure-elevating effect of salt loading.