Mobilization of extracellularly bound Ca2+ during high K+ and norepinephrine stimulation of the rabbit aorta.

The effects of alpha-adrenergic stimulation and high K+-induced membrane depolarization on 45Ca2+ uptake and tension generation in the rabbit aorta were investigated. Tension and unidirectional 45Ca2+ uptake were increased by both stimulants. Moreover, this 'steady-state' uptake remained elevated for as long as the stimulants were present. When tissues were preincubated in 45Ca2+-containing PSS prior to the Ne or high K+ challenge the resulting Ca2+ uptake showed an 'initial burst' of uptake which was not observed in the 'steady-state' experiments. The magnitude of the 'initial burst' increased with time displaying a t1/2 for exchange of 1.25 min for both high K+ and Ne, suggesting that this Ca2+ source is shared by both stimulants. The 'initial burst' became Ca2+ saturated when [Ca2+]o was between 0.5 and 1.5 mM, was enhanced by 45Ca2+ preincubation in a solution of lowered ionic strength and was inhibited (approximately 70%) by D600 (5 X 10(-6) M). In contrast, the 'steady-state' uptake was linearly dependent on [Ca2+]o up to 6.4 mM, was 90% inhibited by 5 X 10(-6) M D600 and was unaffected by lowered ionic strength. It is concluded that the properties displayed by the Ca2+ source responsible for the 'initial burst' and 'steady-state' uptake suggest that they are of distinct origin; the 'initial burst' being derived from a bound extracellular Ca2+ pool and the 'steady-state' uptake resulting from the uptake of free Ca2+ dissolved in the extracellular space.