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Myosin light chain kinase, smooth muscle Adenylate cyclase type 9 PKA complex PKA complex Protein kinase C Beta-2 adrenergic receptor G protein complex Myosin LC-P Myosin light chain 3 Inositol 1,4,5- trisphosphate receptor type 1 Voltage- dependent L-type calcium channel subunit beta-1 Voltage- dependent L-type calcium channel subunit alpha-1C Myosin light chain phosphatase Calmodulin Intermediate conductance calcium- activated potassium channel protein 4 Phospholipase C Guanine nucleotide- binding protein alpha Calmodulin Guanine nucleotide- binding protein G(I)/G(S)/G(T) subunit beta-1 Guanine nucleotide- binding protein G(I)/G(S)/G(O) subunit gamma-12 Voltage- dependent calcium channel subunit alpha-2/delta-1 Carteolol Ca+ Ca+ K+ K+ Ca+ GDP GTP ATP cAMP Inositol 1,4,5-trisphosphate Phosphatidylinositol 4,5-bisphosphate Diacylglycerol GTP Calcium Ca+ Muscle Contraction Muscle Relaxation Magnesium Calcium Manganese Sarcoplasmic Reticulum Cytosol Ciliary Smooth Muscle Cell Carteolol, administered as an eye drop, antagonizes the beta-2 adrenergic receptor. Since the beta-2 adrenergic receptor is antagonized, it does not activated the G(s) signalling cascade. Inactivated PKA does not phosphorylate calcium activated potassium channels causing potassium influx and promoting depolarization. Inactivated PKA does not phosphorylate phospholipase C, allowing for activation of the L-type calcium channels. There is an overall increase in calcium levels in the cytosol. Increased calcium binds readily to calmodulin. The calcium calmodulin complex is able to activate myosin light chain kinase allowing for a high concentration of myosin LC-P and subsequently, smooth muscle contraction. Myosin binds to actin causing the sarcomere filaments to slide resulting in muscle contraction. Actin Filament