ALTERATIONS IN CALCIUM TRANSPORT AND Ca2+-ATPase ACTIVITY IN CARDIAC NUCLEI OF RAT HEART DURING OVERLOAD-INDUCED CARDIAC HYPERTROPHY
压力超负荷性心肌肥厚大鼠心肌细胞核钙转运的改变

The hypertrophy rat model was established by abdominal aortic constriction, and differential centrifugation was used to fractionate the cardiac nuclei. The alterations in Ca2+-ATPase activity and 45Ca2+ uptake as well as intranuclear Ca2+] of the cardiac nuclei were investigated. The Ca2+-ATPase activity in cardiac nuclei was decreased by 51.93% (P<0.001). 45Ca2+ uptake were significantly augmented in the range of 800-1600 nmol/L of incubating free Ca2+], while intranuclear free Ca2+] elevated markedly in the range of 0-1000 nmol/L (P<0.05), as compared with those of control. PKC inhibitor (bisindolylmaleimide 5μmol/L) and CaM inhibitor (calmidazolium 1μmol/L) inhibited while PKA stimulated 45Ca2+ uptake in the normalcardiac nuclei, but the 45Ca2+ uptake in the hypertrophic cardiac nuclei were inhibited only by CaM inhibitor and not affected by PKA and PKC inhibitor. These results suggested that the alterations in calcium transport system in the myocardial nuclei may be partly responsible for the modified cardiac function in pressure overload-induced cardiac hypertrophy, while they also might be regulated by PKA, CaM and PKC.