Control of motility and secretion in the upper GI Flashcards
(37 cards)
Components of the ENS
myenteric plexus (between two external muscle coats) submucosal plexus (submucosa, small and large intestine only)
Outputs of ENS & ANS
muscularis externa
muscularis mucosae
exocrine/endocrine cells
Muscularis externa
By myenteric plexus
Controls motility: tonic contraction, rhythmic segmentation, oscillatory movements, peristalsis
Muscularis mucosae
By submucosal plexus further mixing (movement of the villi)
Role of hormones in GI motility
Modulate responses to ICCs and their impact on the intracellular calcium concentration during initiation of a slow wave
Influence resting contractility of muscle in the upper GI
Secretory components of the stomach
gastrin (endocrine)
histamine (endocrine)
ACh (ENS)
Enterochromaffin-like cell
Modulated by gastrin and ACh of ENS to produce histamine to trigger the release of acid, in addition to their own effects on parietal cells
Enteric intrinsic interneurons
influence acid secretion by parietal cells directly
secretion of gastrin through GRP (would also increase acid secretion by parietal cells)
in the cepahlic, gastric, and intestinal phases of stimulation of gastric secretion
Enterogastric reflex
certain substances are sensed in the duodenum, then enterogastrones (hormones) are released as a reflex that travels through the celiac ganglions to the effectors in the stomach
Myenteric (Auerbach’s) plexus
within muscularis externa, between two layers of muscle
Sensory: receptors in gut wall that senses mechanical, chemical or thermal stimuli, then relates signal to interneurons within ganglia
Interneurons receive from sensory then transmits to motor neurons, which innervate the smooth muscle, exocrine and endocrine/parietal cells
Submucosal (Meissner’s) plexus
located in the submucosa
Similar reflex as myenteric (sensory –> motor), except only a small number of innervates the smooth muscle layer (muscularis mucosae)
NTs in longitudinal layers of the muscularis externa
Excitatory: ACh
Inhibitory: NO, vasoactive intestinal peptide, purines (ATP, beta-NAD)
NTs in circular layers of the muscularis externa
Excitatory: ACh, substance P, serotoninin (5-HT)
Inhibitory: NO, vasoactive intestinal peptide, purines (ATP, beta-NAD)
Submucosal plexus NT
Stimulatory: ACh (motility), VIP (glandular/exocrine)
Regulates secretion
Regulates motility of the muscularis mucosae
Co-localization
neurons that contain more than one type of NT
Secretomotor neuron
neuron that is able to induce a gland to secrete a substance
Slow wave
Spontaneous rhythmic fluctuations in the RMP intrinsic to the GI tract
1-5 s/oscillation
frequency (region-specific): distal stomach - 3 cycles/min, duodenum - 12 cycles/min
Determine the fq of phasic smooth muscle contractile events
Tonic contraction (tone)
muscularis externa circular muscle contractions that functionally separate different areas of the GI tract
allows for unidirectional movement
Sphincter
site of prolonged tonic contraction
ensures unidirectional movement
RMP in the GI tract
-40 to -80 mV
Determined by: Na and K channels, Na/K ATPase
Phases of a slow wave
Rising phase: entry of Ca through CaV channels and others, and release from intracellular storage
Repolarization: activation of Ca-dependent K channels, concominant reduction in cytosolic Ca
Plateau: due to inward Ca current and outward K fluxes
Spike potentials
contraction begins when electrical threshold is reached for opening of CaV channels
In some regions: spike action potentials are also generated, results in larger Ca influxes through CaV –> greater contractions
Interstitial Cells of Cajal (ICC)
Pacemaker cells
concentrated in myenteric plexus (ICCMY) and muscle (ICCMI)
ICCMY responsible for generating and propagating slow waves (Ca oscillations)
Gap junctions allow for electrical coupling
Factors that contribute to Ca influx in GI tract (6)
- CaV (L-type) - predominant
- Store-operated Ca channels (SOCs) - open in response to depletion of intracellular Ca
- Stretch-activated Ca channels
- NTs and hormones acting on receptors coupled to activation of phospholipase C and release of IP3, resulting in release of intracellular Ca (ACh, substance P)
- Receptor-operated Ca channels (ROCC)
- Ca ATPases, Na/Ca exchangers: extrude Ca following contractions, also reuptake into intracellular storage