Analytical studies of spontaneous and vasopressin-induced calcium oscillations in cultured vascular smooth muscle cells.
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.
Department of Medical Education and Research, Kaohsiung-Veterans General Hospital, Taiwan. shenga@cc.nsysu.edu.tw
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D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001013:Aorta, Thoracic / Q000033:anatomy & histology / Q000378:metabolism; D002118:Calcium / Q000378:metabolism* / Q000502:physiology; D002478:Cells, Cultured; D004594:Electrophysiology; D006146:Guanidines / Q000494:pharmacology; D008954:Models, Biological; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009991:Oscillometry / Q000379:methods*; D020110:Pinacidil; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology; D014667:Vasopressins / Q000494:pharmacology*
D006146:Guanidines; D015221:Potassium Channels; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D014667:Vasopressins; D020110:Pinacidil; D000255:Adenosine Triphosphate; D002118:Calcium