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Modulation of vasa recta calcium activated chloride channels by myosin light chain kinase

Descending vasa recta (DVR) are 12 ‐ 15 μm microvessels that supply the renal medulla with blood flow. They consist of contractile smooth muscle like pericytes and an endothelial monolayer. DVR pericytes express calcium activated chloride channels (ClCa). In this study, we tested whether myosin light chain kinase regulates those channels. Using the conventional whole cell patch‐clamp technique, ClCa currents were elicited in murine pericytes by depolarizing the cells during EGTA buffering of intracellular Ca2+ to a range between 20 to 1000 nM. Pericytes, held at ‐80 mV and depolarized from ‐90 mV to +80 mV in 10 mV increments, showed outwardly rectifying ClCa currents that were both voltage and Ca2+ dependent. The ClCa currents did not rundown after initial access via ruptured patches. ClCa currents elicited in the presence of 500 nM intracellular Ca2+ were significantly inhibited by intracellular or extracellular application of the calmodulin inhibitor W‐7 (30 μM). Selective myosin light chain kinase (MLCK) inhibitors, ML‐7 or ML‐9 also inhibited ClCa currents in a concentration dependent manner. Finally, the MLCK inhibitor ML‐7 (20 μM), reversed AngII (10 nM) induced pericyte depolarization and dilated AngII preconstricted DVR. In conclusion, DVR pericyte ClCa currents, membrane potential and contraction by AngII are regulated by calmodulin and myosin light chain kinase.