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. 2016 Jan 26;4(2):e12692. doi: 10.14814/phy2.12692

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© 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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A model summarizing smooth muscle signaling pathways that are regulated by RGS2 to control uterine artery myogenic tone. Under conditions where RGS2 is absent or deficient, G protein activation by mechanosensation leads to a sustained phospholipase C (PLC)‐mediated Ca²⁺ release from the sarcoplasmic reticulum (SR), which increases cytosolic Ca²⁺ concentration and activates Ca²⁺‐Cam/MLCK‐mediated smooth muscle contraction. High cytosolic Ca²⁺ due to the absence/deficiency of RGS2 also inhibits SR Ca²⁺ release via ryanodine receptors (RyR), which normally inhibits contraction by promoting membrane hyperpolarization. Cam, calmodulin; MLCK, myosin light‐chain kinase; BK_C _a ²⁺, Ca²⁺‐activated potassium channel; myosin‐P, phosphorylated myosin.