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Smooth muscle relaxation in the gastrointestinal tract refers to a physiological process modulated by enteric neurotransmitters, including nitric oxide (NO) and purines (e.g., ATP), which act through their respective receptors to reduce contractility of GI smooth muscle cells[3][4]. The primary molecular target mediating NO-induced relaxation is the soluble guanylyl cyclase (sGC, also called the nitric oxide receptor), which, when activated by NO, increases cellular cGMP, ultimately leading to activation of protein kinase G and myosin light chain phosphatase and resulting in smooth muscle relaxation[3][4]. The purinergic P2Y1 receptor, a G protein-coupled receptor responsive to ATP, also mediates smooth muscle relaxation by activating potassium channels, further hyperpolarizing smooth muscle cells[3]. Thus, "smooth muscle relaxation in gastrointestinal tract" describes a process that centrally involves the sGC and P2Y1 molecular targets, among others.
Activation of sGC increases cGMP levels, which activates protein kinase G, phosphorylates downstream targets, and activates myosin light chain phosphatase, leading to muscle relaxation[3][4]. P2Y1 receptor activation by ATP or analogs opens potassium channels, hyperpolarizes the membrane, and suppresses contraction[3].
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