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

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          The effects of α-adrenergic stimulation and high K<sup>+</sup>-induced membrane depolarization on <sup>45</sup>Ca<sup>2+</sup> uptake and tension generation in the rabbit aorta were investigated. Tension and unidirectional <sup>45</sup>Ca<sup>2+</sup> 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 <sup>45</sup>Ca<sup>2+</sup>-containing PSS prior to the Ne or high K<sup>+</sup> challenge the resulting Ca<sup>2+</sup> 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<sub>½</sub> for exchange of 1.25 min for both high K<sup>+</sup> and Ne, suggesting that this Ca<sup>2+</sup> source is shared by both stimulants. The ‘initial burst’ became Ca<sup>2+</sup> saturated when [Ca<sup>2+</sup>]<sub>o</sub> was between 0.5 and 1.5 mM, was enhanced by <sup>45</sup>Ca<sup>2+</sup> preincubation in a solution of lowered ionic strength and was inhibited (∼70%) by D600 (5 × 10<sup>–6</sup> M). In contrast, the ‘steady-state’ uptake was linearly dependent on [Ca<sup>2+</sup>]<sub>o</sub> up to 6.4 mM, was 90% inhibited by 5 × 10<sup>–6</sup> M D600 and was unaffected by lowered ionic strength. It is concluded that the properties displayed by the Ca<sup>2+</sup> 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 Ca<sup>2+</sup> pool and the ‘steady-state’ uptake resulting from the uptake of free Ca<sup>2+</sup> dissolved in the extracellular space.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          23 September 2008
          : 22
          : 5
          : 234-243
          Department of Pharmacology, University of Miami Medical School, Miami, Fla., USA
          158607 Blood Vessels 1985;22:234–243
          © 1985 S. Karger AG, Basel

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          Pages: 10
          Research Paper


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