Key result
Lanthanum inhibited passive 45Ca uptake in cultured porcine aortic endothelial cells, and passive uptake increased progressively as extracellular pH was raised from 5.2 to 9.2.
The study characterizes a calcium-leak pathway in porcine aortic endothelial cells that is sensitive to lanthanum and pH, potentially regulating the release of endothelium-derived relaxing factors.
No immediate clinical implications from porcine cell data; leaves open endothelial calcium-leak pathway contributions to vascular tone.
Unidirectional 45Ca fluxes were measured to characterize the calcium-leak pathway in cultured endothelial cells of pig aorta. Lanthanum, but not other calcium channel blockers such as verapamil and diltiazem, inhibited the passive 45Ca uptake. Passive uptake of 45Ca across the plasma membrane increased progressively as extracellular pH was raised from 5.2 to 9.2. SK&F 96365, a putative inhibitor of receptor-mediated Ca2+ entry, selectively blocked ATP-induced 45Ca uptake. The Ca2+ leak pathway may play an important role in endothelial cell Ca2+ homeostasis which controls the basal and stimulated release of endothelium-derived relaxing factors (i.e., EDRF, prostacyclin) in physiological or pathological situations.
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Laskey et al. (1993) studied Cultured porcine aortic endothelial cells. Lanthanum, extracellular pH changes, and SK&F 96365 was evaluated on Unidirectional 45Ca fluxes and passive 45Ca uptake. Lanthanum inhibited passive 45Ca uptake in cultured porcine aortic endothelial cells, and passive uptake increased progressively as extracellular pH was raised from 5.2 to 9.2.
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