Figure 6.

Increased Ca²⁺ release from internal stores mediates augmented myogenic tone in RGS2 deficient mice. (A & B) Myogenic response of uterine arteries from wild type (Rgs2+/+) and Rgs2 knockout (Rgs2−/−) mice in the absence and presence of ryanodine (Ryan, closed triangles), thapsigargin (Thaps, open diamonds), or Ryan plus N,N,N′,N′‐tetrakis(2‐pyridylmethyl)ethane‐1,2‐diamine (Ryan + TPEN, open squares). Thaps and Ryan + TPEN almost completely blocked myogenic response in both genotypes. (C) Depletion of extracellular Ca²⁺ with Ca²⁺‐free PSS induces robust Ca²⁺ release from internal stores in uterine artery smooth muscle cells (SMCs) from Rgs2 knockout (Rgs2−/−, open circles) relative and wild‐type (Rgs2+/+, closed circles) mice. Ionomycin induces Ca²⁺ release from internal stores in SMCs from both genotypes. (D) Ca²⁺‐free PSS but not ionomycin‐induced Ca²⁺ release from internal stores is almost completely abolished by Ryan in SMCs from Rgs2−/− mice. (E) A plot of area under the curve (AUC) of fura‐2 fluorescence shown in C and D. Note the augmentation of ionomycin‐induced Ca²⁺ response by Ryan in Rgs2+/+ SMCs, which correlates with enhanced myogenic response in Rgs2+/+ uterine arteries in the presence of Ryan in A. Values are mean ± SE. *^,**P < 0.05, 0.01; ^## P < 0.01 versus corresponding Rgs2+/+.