The external aldosterone regulating on the rat cardiac calcineurin
- VernacularTitle:外源性醛固酮调控大鼠心肌钙调神经磷酸酶的研究
- Author:
Xiaohua XIE
;
Lianqing CHANG
;
We CHEN
- Publication Type:Journal Article
- Keywords:
aldosterone;
calcineurin;
nitric oxide;
endothelin;
spironolactone
- From:
Medical Journal of Chinese People's Liberation Army
2001;0(09):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the changes of the activity and the distribution of the rat cardiac calcineurin (CaN) which is the signalling molecule of the hypertrophy induced by the external aldosterone(Ald), and to detect the mechanism of the regulation of CaN. Methods 21 male wister rats were randomly divided into 3 groups: group Ald(7 rats), treated with Ald 18?g/d, peritoneal injection (i p) for 4 weeks; group spironolactone (spiron) (7 rats), treated with Ald and with spiron 20mg?kg -1 ?d -1 oral for 4 weeks; and group control (7 rats). The plasma concentrations of Ald, angiotensin Ⅱ(Ang Ⅱ)and endothelin(ET), blood levels of NO, the tissue activity of the CaN and distribution of CaN A? in the myocardium of the left ventricle, were detected in the rats by the radioimmunoassay , by the nitrate assay, by the chromophoric assay and by the immunohistochemistry, respectively. Results The concentration of the plasma Ald increased by 1 62 times, the blood NO - 3 concentration was deceased, the ratio of Ald over NO - 3( Ald/ NO - 3) increased by 2 95 times, and the cardiac tissue levels of CaN activity was were 1 47 times higher, in the rats treated with ald than in the normotensive rats. CaN A? distributed over cardiac cytoplasm, and the positive dyeing of the local CaN A? in the cytoplasm was thick near the cell membrane in the rats treated with Ald. The treatment with spiron could decreased the blood levels of the AngII?Ald/ NO - 3?ET/NO - 3?AngII/ NO - 3 and the tissue activity of myocardial CaN, positive dyeing of the local CaN A? in the cytoplasm, and increased blood NO - 3 concentration. Conclusion The aldosterone may be the main stimuli factor which can damage the balance of the blood active factors, and then make a novel cardiac hypertrophic signalling molecule calcineurin activated and redistributed in the cytoplasm of the rat left ventricular myocardium
