Figure 3.

Pulmonary arterial hypertension (PAH) increases basal and thapsigargin (thaps)–evoked Ca²⁺ signals. A: Histograms of baseline Ca²⁺ event distributions with respect to event duration show distinct, right-shifted distributions for wild-type (wt), TRPC4-knockout (ko), hypertensive wild-type (wt PAH), hypertensive TRPC4-knockout (ko PAH) groups. B: Histograms of event distributions versus event duration after stimulation with thapsigargin reveal similarly right-shifted distributions compared with baseline, with an expanded maximum event number within the wild-type hypertensive group. C: Intracellular Ca²⁺ event numbers are quantified as bar charts. Basal (bl) responses (open bars) show a significant increase in the number of events in hypertension (wt PAH) relative to control (wt). TRPC4 inactivation (ko PAH) recovers this response. Thapsigargin-stimulated cell responses (closed bars) are also significantly increased in PAH groups, and partially abolished after TRPC4 inactivation. D: Signal half maximum duration measurements are not significantly different between all groups basally (open bars), but PAH cell response duration after thapsigargin stimulation is significantly reduced relative to normotensive control. n = 3 to 4 for all groups (C and D). ^∗P < 0.05, ^∗∗P < 0.01.