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Smooth Muscle Relaxation and Contraction in the Gastrointestinal System

Full Title: The Mechanism of Smooth Muscle Relaxation and Contraction in the Gastrointestinal System: Autonomic Signaling and Motility

Author: Cheryl Mazzeo

Institutional Affiliation: University of Maine

Location of Work: United States

Year Completed: 2022

Not Submitted for Publications Because: Partially Completed Paper

Topic: Biology

Keywords: Smooth muscle, autonomic signaling, gastrointestinal system, relaxation, contraction, motility, mechanism, neurological signaling



Smooth muscle supports homeostasis in the gastrointestinal (GI) system by facilitating the absorption of nutrients and peristalsis. Defining the mechanism by which autonomic nervous system (ANS) control regulates the relaxation and contraction of smooth muscle cells, and thereby how the GI system and brain communicate, may lead to future clinical development. The sarcoplasm of muscle cells contains Ca2+, which is a key secondary signaling molecule involved in contraction. Synaptic networks allow afferent and efferent communication between the brain and the smooth muscle tissue.

Enteric Nervous System (ENS)

Due to the communication between the gut-brain axis (GBA) and the ENS, corticotropin-releasing factor (CRF) is secreted from the hypothalamus. CRF triggers secretion of adrenocorticotropic hormone (ACTH) from the pituitary, which releases cortisol from the adrenal glands and has a downstream influence on smooth muscle contraction.

Role in GI Motility

Acetylcholine (ACh) is the neurotransmitter responsible for evoking contractions and action potentials (APs) create the necessary force. When adenosine triphosphate (ATP) detaches myosin from the actin filament, the muscle becomes relaxed. However, in the presence of ACh, a positive feedback loop for Ca2+ is observed, driving the downstream binding of myosin that will contract the smooth muscle.

Excitation-Contraction (E-C) Coupling

E-C coupling introduces Ca2+ to, and recovers it from, IP3 (inositol 1,4,5-trisphosphate) receptor-operated stores during contraction. This ion is supplied by voltage-gated calcium channels (VGCC). In the GI system, E-C coupling occurs in response to APs. When receptors are activated, positive feedback produces a higher concentration of IP3, releasing

Ca2+ stores and activating protein kinases.


When nitric oxide (NO) and ATP operate together, they interact with the P2Y1 membrane receptor to relax smooth muscle. Patients with GI dysmotility due to spinal damage may experience a physiologic inhibition of organ functionality. Applying therapy to inactivate K+ and Cl- channels while enhancing Ca2+ activity may restore the activity of non-functioning tissue.


Steps of the proposed mechanism may allow for future developments in therapy for GI motility complaints. The proposed mechanism synthesizes and previously reported findings and proposes how broad models for smooth muscle activation can be applied to the GI tract.

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