Mobilization of Extracellularly Bound Ca ²⁺ during High K ⁺ and Norepinephrine Stimulation of the Rabbit Aorta

Abstract

The effects of α-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 preincu-bated 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 t_½ 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 (∼70%) by D600 (5 × 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 × 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.