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GIT Physiology: Enteric Nervous System, Electrical Activity, Hormones, Circulation, and Deglutition

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1. Components of the Enteric Nervous System (ENS)

1. Myenteric plexus (Auerbach's plexus) — outer plexus
2. Submucosal plexus (Meissner's plexus) — inner plexus

Ganong's Review of Medical Physiology, 26th ed.; Guyton and Hall Textbook of Medical Physiology

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2. Myenteric Plexus — Location and Significance

• Primary controller of GIT motility — peristalsis and mixing contractions
• Peristalsis is absent or markedly weakened in segments where the myenteric plexus is congenitally absent (e.g., Hirschsprung disease)
• Blocked by atropine (anticholinergic), confirming its cholinergic nature
• Mediates the myenteric reflex (law of the gut): when a segment is distended, the plexus creates contraction proximal to the bolus and receptive relaxation distal to it, propelling contents aborally
• Postganglionic parasympathetic neurons are located within this plexus — parasympathetic stimulation increases its activity

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3. Meissner's Plexus (Submucosal Plexus)

• Senses the environment of the intestinal lumen (chemical, osmotic, mechanical)
• Regulates gastrointestinal secretion and absorption by acting on secretory cells
• Controls local GIT blood flow
• Regulates epithelial cell function

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4. Comparison: Myenteric vs. Meissner's Plexus

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5. Sympathetic and Parasympathetic Control of GIT

Parasympathetic (Excitatory — "rest and digest")

• Cranial division: Vagus nerve (CN X) → innervates esophagus, stomach, pancreas, and intestines to the first half of the large intestine
• Sacral division: S2–S4 via pelvic nerves → distal half of large intestine, sigmoid, rectum, anus (controls defecation reflexes)
• Postganglionic neurons are located in the myenteric and submucosal plexuses
• Effect: Stimulation increases activity of the entire ENS → enhanced peristalsis, increased secretion, relaxed sphincters, increased mucosal blood flow
• Parasympathetic nerves to stomach and lower colon also increase local blood flow secondary to enhanced glandular activity

Sympathetic (Inhibitory — "fight or flight")

• Preganglionic fibers arise from T5–L2 spinal cord segments
• Pass through sympathetic chains to celiac ganglion and mesenteric ganglia; postganglionic fibers spread throughout the gut
• Postganglionic endings release norepinephrine
• Effects:
  1. Direct inhibition of intestinal smooth muscle by norepinephrine
  2. Inhibition of enteric nervous system neurons (reduces all GIT activity)
• Strong sympathetic stimulation can literally block movement of food through the tract
• Causes vasoconstriction of GIT arterioles and large veins (redistributes blood to vital organs during shock or exercise)

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6. Gastrointestinal Reflexes

Type 1 — Intrinsic Gut Wall Reflexes (entirely within the ENS)

• Control secretion, peristalsis, mixing contractions, local inhibition
• Example: Myenteric (peristaltic) reflex — distension triggers contraction behind + relaxation ahead → aborad propulsion

Type 2 — Gut → Prevertebral Sympathetic Ganglia → Gut

• Transmit long-distance signals between regions of the GIT
• Gastrocolic reflex: signals from stomach → colon → evacuation of colon (after a meal)
• Enterogastric reflex: signals from colon/small intestine → inhibit gastric motility and secretion
• Colonoileal reflex: signals from colon → inhibit emptying of ileal contents into colon

Type 3 — Gut ↔ Spinal Cord or Brain Stem

• Gastric reflexes via vagus: stomach/duodenum → medulla → back to stomach → controls motor and secretory activity
• Pain reflexes: intense irritation → general inhibition of entire GIT
• Defecation reflexes: colon/rectum → spinal cord → powerful colonic, rectal, and abdominal wall contractions

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7. Mechanism of Slow Wave Development

• Amplitude: 5–15 mV
• Frequency: 3/min (stomach body) → up to 13/min (duodenum) → 8–9/min (terminal ileum)
• Generated by interstitial cells of Cajal (ICC) — specialized pacemaker cells that form a network interposed between muscle layers, with synaptic-like contacts to smooth muscle

1. ICC possess unique ion channels that periodically open and produce inward (pacemaker) currents
2. These cyclic changes in ICC membrane potential are transmitted to adjacent smooth muscle via gap junctions
3. The result is a rhythmic, slow undulation in the resting potential of the smooth muscle (−50 to −60 mV baseline)
4. During slow waves, mainly sodium ions enter — calcium entry is minimal, so slow waves alone usually do not cause muscle contraction

Guyton and Hall Textbook of Medical Physiology

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8. Mechanism of Spike Potential Development

• When a slow wave peak raises the membrane potential above the threshold of approximately −40 mV, spike potentials are triggered
• The higher the slow wave peak, the greater the frequency of spikes (1–10 spikes/second)
• Unlike nerve action potentials (which use fast Na⁺ channels), GIT spike potentials use slow calcium-sodium (Ca²⁺/Na⁺) channels:
  • Large influx of Ca²⁺ + smaller influx of Na⁺
  • Slow channel kinetics → long spike duration (10–20 ms vs. ~1 ms in nerves)
• The Ca²⁺ entry during spikes activates the calmodulin–myosin pathway → smooth muscle contraction
• Slow waves set the timing and rhythm; spike potentials determine contraction strength

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9. Factors that Depolarize and Hyperpolarize the GIT Membrane

Depolarizing Factors (increase excitability → more likely to contract):

1. Stretching of the smooth muscle
2. Acetylcholine released from parasympathetic nerve endings
3. Specific gastrointestinal hormones (e.g., gastrin, motilin)

Hyperpolarizing Factors (decrease excitability → less likely to contract):

1. Norepinephrine or epinephrine acting on the fiber membrane
2. Sympathetic nerve stimulation (releases norepinephrine)

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10. Neurotransmitters of the Enteric Nervous System

Excitatory Neurotransmitters:

Inhibitory Neurotransmitters:

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11. Gastrointestinal Hormones

• Somatostatin — inhibits most GIT hormones and secretions
• VIP — inhibitory; vasodilation, secretion
• Glucagon-like peptide-1 (GLP-1) — incretin; slows gastric emptying

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12. Effect of Gut Activity and Metabolic Factors on GIT Blood Flow (Splanchnic Circulation)

Relationship Between Activity and Blood Flow:

• Blood flow in each GIT region is directly proportional to local activity level
• During active nutrient absorption, villous blood flow increases up to 8-fold
• After a meal, blood flow increases greatly, returning to resting over 2–4 hours

Mechanisms of Increased Blood Flow During GIT Activity:

1. Vasodilator hormones released from gut mucosa during digestion: CCK, VIP, gastrin, secretin — same hormones that control GIT motor and secretory activity
2. Kinins (kallidin and bradykinin) released by gastrointestinal glands at the same time as secretion → potent vasodilators
3. Decreased O₂ tension in the gut wall during active digestion → local metabolic vasodilation
4. Increased CO₂, lactic acid, adenosine from active tissue — contribute to arteriolar dilation
5. Severe prolonged ischemia → mucosal damage → impaired absorptive capacity

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13. Nervous Control of GIT Blood Flow / Splanchnic Circulation

Parasympathetic Control:

• Stimulation of parasympathetic nerves to the stomach and lower colon → increases local blood flow, but this is secondary to increased glandular secretory activity, not a direct effect
• Increased secretion → increased metabolic demand → metabolic vasodilation

Sympathetic Control:

• Sympathetic stimulation → direct vasoconstriction of GIT arterioles → greatly decreased blood flow
• After a few minutes of vasoconstriction, "autoregulatory escape" occurs if stimulation is not too severe — local metabolic vasodilator mechanisms override sympathetic vasoconstriction to preserve nutrient flow

• During heavy exercise: diverts splanchnic blood to skeletal muscle and heart
• During circulatory shock: protects brain and heart by severely reducing GIT flow (can reduce to very little for hours)
• Sympathetic constriction of large mesenteric veins displaces 200–400 mL of blood into systemic circulation — critical in hemorrhagic shock

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14. Mastication (Chewing) — Reflex Arc and Importance

Innervation:

• Jaw muscles are innervated by the motor branch of cranial nerve V (trigeminal nerve)
• Chewing controlled by reticular nuclei in the brain stem
• Can also be initiated from hypothalamus, amygdala, and cerebral cortex (near taste/smell areas)

Reflex Arc of Mastication (Chewing Reflex):

Food bolus in mouth
        ↓
Pressure/stretch stimulates oral mucosa mechanoreceptors
        ↓
Afferent: CN V (trigeminal sensory)
        ↓
Brain stem chewing center (reticular formation)
        ↓
Reflex inhibition of jaw-closing muscles → jaw drops
        ↓
Stretch of jaw muscles → stretch reflex → rebound contraction
        ↓
Jaw closes, compresses bolus against oral mucosa
        ↓
Oral mucosa stimulated again → repeat cycle

Importance of Chewing:

1. Breaks indigestible cellulose membranes around plant cell nutrients (especially fruits and raw vegetables)
2. Increases surface area for digestive enzymes (enzymes act only on particle surfaces)
3. Grinds food to fine particles → prevents excoriation of GIT mucosa
4. Facilitates gastric emptying and transit through all GIT segments
5. Initiates salivary enzyme (amylase) digestion of carbohydrates
6. Forms a bolus suitable for swallowing

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15. Stages of Swallowing (Deglutition)

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16. Voluntary Stage of Swallowing — Mechanism

1. The tongue voluntarily squeezes and rolls the bolus posteriorly into the pharynx by pressing the tongue upward and backward against the hard palate
2. Once the bolus passes into the posterior pharynx, the swallowing process becomes entirely involuntary and cannot be stopped

• The bolus stimulates epithelial swallowing receptor areas around the pharyngeal opening, especially the tonsillar pillars
• Afferent impulses travel to the swallowing center in the medulla (reticular formation)
• This initiates the coordinated sequence of the pharyngeal stage

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Pharyngeal Stage (for completeness):

1. Soft palate elevation → closes posterior nares (prevents nasal reflux)
2. Palatopharyngeal folds approximate → form sagittal slit (filters large food particles)
3. Vocal cords approximate; larynx pulled upward and forward → epiglottis swings over laryngeal opening (airway protection)
4. Upper esophageal sphincter relaxes → food moves from pharynx into upper esophagus
5. Peristaltic contraction begins in superior pharyngeal constrictor → sweeps bolus downward (lasts ~1–2 seconds)
6. Respiration is inhibited during this stage

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