During excitation-contraction coupling, calcium is released by the tubules of the SR, but as mentioned above, it also moves into the cell via membrane channels from the extracellular space. By binding to troponin, calcium ions activate myosin in all striated muscle types, but in smooth muscle, they activate calmodulin, a cytoplasmic calcium-binding protein. Calmodulin, in turn, interacts with a kinase enzyme called myosinkinase or myosin light chain kinase which phosphorylates the myosin, activating it. (Note that this is just one pathway of smooth muscle activation. There are others. For example, in some smooth muscles, regulatory proteins associated with actin appear to play a role. ) Recall that all somatic nerve endings, that is, nerve endings that serve skeletal muscle, release acetylcholine, which excites the skeletal muscle. However, different autonomic nerves serving the smooth muscle of visceral organs release different neurotransmitters, each of which may excite or inhibit a particular group of smooth muscle cells. The effect of a specific neurotransmitter on a given smooth muscle cell depends on the type of receptor molecules on its sarcolemma. For example, when acetylcholine binds to ACh receptors on smooth muscle in the bronchioles (small air passageways of the lungs), the muscle contracts strongly, narrowing the bronchioles. When norepinephrine, released by a different type of autonomic nerve fiber, binds to norepinephrine receptors on the same smooth muscle cells, the effect is inhibitory, so the muscle relaxes, dilating the air passageways. However, when norepinephrine binds to smooth muscle in the walls of most blood vessels, it stimulates the smooth muscle cells to contract and constrict the vessel.