Cao Chun-Mei, Xia Qiang, Fu Chen, Jiang Hui-Di, Ye Zhi-Guo, Shan Yue-Liang, Chan Jun-Zhu
Department of Physiology, Department of Cardiology of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310031.
Sheng Li Xue Bao. 2003 Feb 25;55(1):83-90.
The purpose of the present study was to investigate whether interleukin-2 (IL-2) changes the activity of sarcoplasmic reticulum (SR) Ca(2+) ATPase, sarcolemmal Ca(2+)ATPase and Na(+)/K(+) ATPase by measuring the Pi liberated from ATP hydrolysis with colorimetrical methods. It was shown that the activity of Ca(2+)ATPase in SR from IL-2-perfused (10, 40, 200, 800 U/ml) rat heart increased dose-dependently. After incubation of the SR with ATP (0.1 approximately 4 mmol/L), the activity of SR Ca(2+)ATPase increased dose-dependently in the control group. In the SR from 200 U/ml IL-2-perfused hearts, the activity of Ca(2+)ATPase was much higher than that in the control group. On the other hand, incubation of the SR with Ca(2+) (1 approximately 40 micromol/L) increased the activity of SR Ca(2+) ATPase in the control group. The activity of SR Ca(2+)ATPase of IL-2-perfused hearts was inhibited as the function to Ca(2+). Pretreatment with specific kappa-opioid receptor antagonist nor-BNI (10 nmol/L) for 5 min attenuated the effect of IL-2 (200 U/ml) on the activity of SR Ca(2+) ATPase. After pretreatment with pertussis toxin (PTX, 5 mg/L) or U73122 (5 micromol/L), IL-2 failed to increase SR Ca(2+)ATPase activity. The activity of SR Ca(2+)ATPase was not changed by incubation of SR isolated from normal hearts with IL-2. Perfusion of rat heart with IL-2 did not affect the activity of sarcolemmal Ca(2+)ATPase and Na(+)/K(+)ATPase. It is concluded that perfusion of rat heart with IL-2 increases the activity of SR Ca(2+)ATPase dose-dependently, which is mainly mediated by cardiac kappa-opioid receptor pathway including a PTX sensitive Gi-protein and phospholipase C. IL-2 increases the activity of SR Ca(2+)ATPase as the function to ATP, but inhibits the activity of SR Ca(2+)ATPase as the function to Ca(2+). IL-2 has no effect on the activity of sarcolemmal Ca(2+)ATPase and Na(+)/K(+)ATPase.
本研究的目的是通过比色法测量ATP水解释放的无机磷酸，来研究白细胞介素-2（IL-2）是否会改变肌浆网（SR）Ca(2+)ATP酶、肌膜Ca(2+)ATP酶和Na(+)/K(+)ATP酶的活性。结果表明，用IL-2（10、40、200、800 U/ml）灌注大鼠心脏后，SR中Ca(2+)ATP酶的活性呈剂量依赖性增加。用ATP（0.1至4 mmol/L）孵育SR后，对照组中SR Ca(2+)ATP酶的活性也呈剂量依赖性增加。在来自用200 U/ml IL-2灌注心脏的SR中，Ca(2+)ATP酶的活性远高于对照组。另一方面，用Ca(2+)（1至40 μmol/L）孵育SR可增加对照组中SR Ca(2+)ATP酶的活性。用IL-2灌注心脏的SR中Ca(2+)ATP酶的活性作为对Ca(2+)的函数被抑制。用特异性κ-阿片受体拮抗剂nor-BNI（10 nmol/L）预处理5分钟可减弱IL-2（200 U/ml）对SR Ca(2+)ATP酶活性的影响。用百日咳毒素（PTX，5 mg/L）或U73122（5 μmol/L）预处理后，IL-2未能增加SR Ca(2+)ATP酶的活性。用IL-2孵育从正常心脏分离的SR，其Ca(2+)ATP酶的活性未改变。用IL-2灌注大鼠心脏不影响肌膜Ca(2+)ATP酶和Na(+)/K(+)ATP酶的活性。结论是，用IL-2灌注大鼠心脏可使SR Ca(2+)ATP酶的活性呈剂量依赖性增加，这主要由包括PTX敏感的Gi蛋白和磷脂酶C的心脏κ-阿片受体途径介导。IL-2作为对ATP的函数增加SR Ca(2+)ATP酶的活性，但作为对Ca(2+)的函数抑制SR Ca(2+)ATP酶的活性。IL-2对肌膜Ca(2+)ATP酶和Na(+)/K(+)ATP酶的活性没有影响。
