Fig. 2. (A) HEK CaR cells were stimulated with 1 mM spermine in the absence of extracellular Ca²⁺. Addition of 100 nM HgCl₂ produced a rapid and reversible block of Ca²⁺ spiking. (B) Pretreatment with 100 nM HgCl₂ did not stimulate HEK CaR cells by itself or prevent the release of Ca²⁺ from internal stores induced by 1 mM spermine. (C) Oscillations resulting from stimulation with carbachol (CCh; 100 µM) and ATP (100 µM) were not blocked by 100 nM HgCl₂ in HEK CaR cells. These records also illustrate that Hg²⁺ is an effective blocker of the PMCA in HEK CaR cells, since the time to return to baseline following Ca²⁺ removal (in the presence of agonists) was significantly attenuated by HgCl₂. (D) Ca²⁺ spiking was not abolished by 100 nM HgCl₂ in HEK WT cells stimulated with 10 µM carbachol. (E) Spermine-induced oscillations were attenuated by 1 mM orthovanadate in HEK CaR cells. (F) Vanadate produced one of two effects on carbachol-stimulated oscillations in HEK WT cells. Shown here are cells in which 1 mM vanadate had little or no action on oscillations (42% of cells). (G) Vanadate (1 mM) sometimes produced an elevated plateau of Ca²⁺ when added acutely to carbachol-stimulated HEK WT cells (58% of cells). (H) 2 mM Caloxin 2A1, a peptide inhibitor of the PMCA, blocked oscillations elicited by NPS R-467 (5 µM).

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