Functional Expression of TRPV4 Channels in Human Collecting Duct Cells: Implications for Secondary Hypertension in Diabetic Nephropathy

Figure 2

Changes in [Ca²⁺]_𝑖 in HCD-cells evoked by mechanical stimulation. In the presence of extracellular calcium (a control), mechanical stimulation of an individual cell, within a cluster, elicits an increase in [Ca²⁺]_𝑖. The rise in [Ca²⁺]_𝑖 rapidly propagates into coupled cells. Removal of extracellular calcium (b) reduces the basal-to-peak change in mechanically evoked [Ca²⁺]_𝑖, but does not negate the response. Depletion of Ca²⁺ stores via preincubation of the Ca²⁺-ATPase inhibitor, thapsigargin (Tg 1 𝜇M; 30 min, (c) in the absence of extracellular calcium, completely prevents mechanically evoked changes in [Ca²⁺]_𝑖. (d) shows mean basal-to-peak data from several experiments (𝑛=4) and indicates a role for both intra- and extracellular calcium in mediating mechanically evoked Ca²⁺-signalling in HCD-cells. Data is represented as an estimated change in [Ca²⁺]_𝑖 recorded as a ratio of 340/380 nm excitation for fura-2. Statistical analysis ((d); 𝑃<0.01 control versus Ca²⁺-free and 𝑃<0.001 control versus Ca²⁺-free + Tg).