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. 2018 Jun 24;596(16):3531–3552. doi: 10.1113/JP275845

Figure 8. Role of intracellular Ca2+ stores in generating pericyte Ca2+ transients in different microvascular segments.

Figure 8

In a PCA, CPA (10 μm) abolished spontaneous Ca2+ transients in pericytes and increased the basal Ca2+ level (A). In another PCA, caffeine (1 mm) prevented the generation of spontaneous Ca2+ transients in pericytes (B). In a different PCA, tetracaine (100 μm) abolished spontaneous Ca2+ transients in pericytes (C). In a capillary, CPA (10 μm) abolished spontaneous Ca2+ transients in pericytes associated with a rise in the basal Ca2+ level (D). In another capillary, caffeine (1 mm) prevented the generation of spontaneous Ca2+ transients in pericytes (E). In the same capillary, tetracaine (100 μm) abolished spontaneous Ca2+ transients in pericytes (F). In a PCV, CPA (10 μm) prevented the generation of spontaneous Ca2+ transients in pericytes associated with a rise in the basal Ca2+ level (G). In another PCV, caffeine (1 mm) abolished spontaneous Ca2+ transients in pericytes (H). In a different PCV, tetracaine blocked spontaneous Ca2+ transients in pericytes (I). [Color figure can be viewed at http://wileyonlinelibrary.com]