AIM: To explore the relationship between the alteration in gene expression of sarcoplasmic reticulum Ca~(2+)-ATPase (SERCA) and phospholamban (PLB) in spontaneously hypertensive rats (SHR). METHODS: 294 samples of total RNA were obtained from the tissue of ventriculum , aortic smooth muscle, liver and kidney in SHR and normotensive rats (WKY). RNA array was used to determine the mRNA levels of SERCA and PLB. RESULTS: Compared with age-matched WKY rats, the systolic blood pressure increased higher in 6-week-old SHR (P

AIM: To investigate the electrophysiological changes of diabetic myocardium and effects of cyclovirobuxine D (CVB-D) on its electrophysiology. METHODS: Diabetes was induced in male SD rats, using a single injection of alloxan into tail vein. Untreated age-matched animals were used as controls. Animal electrocardiogram (ECG) was recorded by 2 weeks. Effects of CVB-D on isolated right ventricular papillary muscle from experimental diabetic rats and control group were observed by recording the transmembrane potentials with conventional glass microelectrodes. RESULTS: QT intervals in ECG and action potential duration (APD) at all levels were significantly lengthened in myocardium from week 2 of diabetes. Within the concentration of 13.3-63.3 ?mol?L~(-1), CVB-D prologated APD of diabetes in dose-dependent manner and more than that of control. Within the concentration of 33.3-63.3 ?mol?L~(-1), CVB-D depressed RP, APA, V_(max) and OS of diabetes in dose-dependent way and more than that of control. In addition, CVB-D at concentration of 20 ?mol?L~(-1) prologated APD in a time-dependent manner. The most prologation of APD was attained about 40 min in control, while more than 40 min in diabetes. CONCLUSION: The results show that QT intervals in ECG and APD at all levels are significantly lengthened in myocardium from week 2 of diabetes. CVB-D prolongates APD and inhibits RP, APA, OS and V_(max) more in diabetes than in control.

AIM: To investigate the effect of phospholamban antisense RNA (asPLB) on the activity of sarco-endoplasmic reticulum (SR) Ca 2+-ATPase, and the change of intracellular free Ca 2+ concentration ([Ca 2+]i) in rat cardiomyocytes by adeno-associated virus(AAV) vector. METHODS: rAAV-asPLB and rAAV-LacZ were constructed by AAV Helper-Free System. RT-PCR and Western blotting were used to determine the mRNA and protein expression of PLB. The activity of SR Ca 2+-ATPase and the [Ca 2+]i were measured. RESULTS: Compared to controls, the PLB mRNA and protein expression reduced in rat cardiomyocytes transfected with rAAV-asPLB. The activity of Ca 2+-ATPase was increased. In rest state, the level of [Ca 2+]i in rAAV-asPLB transfected group was decreased. The level of [Ca 2+]i was increased when induced by isoproterenol. CONCLUSION: rAAV-asPLB vector disrupts the expression of PLB, enhances the activity of Ca 2+-ATPase, reduces the resting [Ca 2+]i and enhances the isoproterenol-induced [Ca 2+]i.