Spontaneous and vasopressin-induced Ca2+ oscillations in cultured vascular smooth muscle (A7r5) cells were further examined and characterized. Intracellular Ca2+ concentrations ([Ca2+](i)) were measured by use of a high-performance laser cytometer. When the oscillatory patterns in [Ca2+](i) were analyzed with a power spectrum method, about 80% of cells exhibited spontaneous Ca2+ oscillations with the frequency of 0.02-0.5 Hz. Nifedipine abolished these repetitive spikes, whereas pinacidil partially attenuated their amplitude and frequency. When vasopressin (100 nM) was applied to A7r5 cells, there was an initial rise in [Ca2+](i), followed by a delayed sustained increase in [Ca2+](i). The one-pool, nonoscillatory model was employed to fit this biphasic change, and the difference between the observed response and the simulated response was then analyzed with a power spectral method. About 50% of cells were noted to display oscillatory patterns in [Ca2+](i) after sustained increase in [Ca2+](i). The present study indicates that spontaneous Ca2+ oscillations in A7r5 cells are modulated by the activity of ATP-sensitive K+ channels and are not related to pertussis toxin-sensitive GTP-binding protein(s). On the basis of the one-pool, nonoscillatory model, it is suggested that the buffering capacity of internal stores appears to be stronger in the cells with spontaneous Ca2+ oscillations than in those in a quiescent state, and the vasopressin-mediated inhibition of accumulation by internal stores was attenuated when the cells exhibited spontaneous Ca2+ oscillations. The implementation of this minimum kinetic model integrated with a power spectrum method would be an alternative to understand the oscillating behavior in [Ca2+](i).
|Number of pages||7|
|Journal||Journal of biochemistry|
|Publication status||Published - 1996 Jan|
All Science Journal Classification (ASJC) codes
- Molecular Biology