Relationship between contents of ET-1, CGRP, NO in myocardium and cardiac function in chronic renal ischemia of rats caused by abdominal aortic banding
- VernacularTitle:大鼠慢性肾缺血时心肌组织ET-1、CGRP、NO含量与心功能关系的研究
- Author:
Bin FENG
;
Luyue GAI
;
Baoshi HAN
- Publication Type:Journal Article
- Keywords:
Renal artery obstruction;
Myocardium;
Endothelin-1;
Calcitonin gene-related peptide;
Nitric oxide;
Heart function tests
- From:
Journal of Chinese Physician
2009;11(5):594-596
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the relationship between the content of ET-1, CGRP, NO in myocardium and cardiac function in chronic renal ischemia of rats caused by abdominal aortic banding. Methods Male wistar rats (weight 180 - 200g) were randomly divid-ed into 2 groups, operation group (n=30) and sham operation group (n=10). Abdominal aorta ligation between right and left renal ar-tery was made with silk suture in operation group, and the narrow degree of aorta was about 50% which was controlled by ligateing with a syr-inge needle (7#). The aorta was not ligated in sham operation group. After 16 weeks of operation, invasive measurement of blood pressure and cardiac function were performed, and content of ET-1, CGRP and NO in myocardium were determined. Results Compared with sham operation group, the blood pressures of rats in operation group were significantly elevated, with cardiac systolic and diastolic function de-creased and left ventricular mass index increased. After 16 weeks, compared with sham operation group, the content of ET-1 in cardiac tissue were significantly elevated in operation group (P<0.01), while the content of CGRP (P<0.01)and NO (P>0.05)were decreased. There were negative correlation between the content of ET-1 in cardiac tissue and LV +dp/dt max(r = -0.37, P<0. 05). Conclusions In the state of chronic kidney iachemia caused by abdominal aorta ligation, content of ET-1 in cardiac tissues were increased while CGRP and NO were decreased. There were negative correlation between the content of ET-1 in cardiac tissues and LV systolic function.