Mechanism of negative inotropic effect of tumor necrosis factor-alpha on rat myocardium.
- Author:
Chen FU
1
;
Chun-mei CAO
;
Jing ZHANG
;
Qiang XIA
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Calcium; metabolism; Calcium-Transporting ATPases; metabolism; Depression, Chemical; In Vitro Techniques; Male; Myocardial Contraction; drug effects; Myocardium; metabolism; Rats; Rats, Sprague-Dawley; Sodium-Potassium-Exchanging ATPase; metabolism; Tumor Necrosis Factor-alpha; pharmacology
- From: Journal of Zhejiang University. Medical sciences 2003;32(3):181-186
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the mechanism of the negative inotropic effect of tumor necrosis factor-alpha (TNF-alpha) in cardiomyocytes.
METHODSThe spectrofluorometric method was used to verify the calcium handling of the single myocyte. The activities of Ca(2+)-ATPase of sarcoplasmic reticulum (SR) and the activities of Ca(2+)-ATPase and Na(+)/K(+)-ATPase of plasma membrane were measured with colorimetric methods.
RESULTSTNF-alpha at 20 U/ml and 200 U/ml depressed the contractility of ventricular papillary muscle to 91% and 76% of control (P<0.01) respectively, but had no effect on the amplitude of electrically induced calcium transient in single myocyte. TNF-alpha inhibited the responsiveness of SR Ca(2+)ATPase activity to ATP (0.1 - 4 mmol/L) and Ca(2+) (1 - 40 micromol/L). TNF-alpha did not alter the activities of Ca(2+)-ATPase and Na(+)/K(+)-ATPase of plasma membrane compared with control group.
CONCLUSIONTNF-alpha decreases the myocardial contractility, at least partly, by inhibiting the activity of SR Ca(2+)- ATPase.
