electrical activity of gastrointestinal smooth muscle
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Electrical Activity of Gastrointestinal Smooth Muscle. The GI smooth muscle acts as a functional syncytium. Characteristic features of the basic electrical activity of GIT & its relation to smooth muscle contractile activity under physiologic conditions. - PowerPoint PPT PresentationTRANSCRIPT
ELECTRICAL ACTIVITY OF GASTROINTESTINAL SMOOTH MUSCLE
• The GI smooth muscle acts as a functional syncytium.
Characteristic features of the basic electrical activity of GIT & its relation to smooth muscle
contractile activity under physiologic conditions
Characteristic features of the basic electrical activity of GIT
• Slow waves spike potential• Spike potentials
• Voltage of the resting membrane potential of the gastrointestinal smooth muscle can be made to change to different levels
Slow Waves• Rhythmical changes in membrane potential
caused by variations in sodium conductance • Slow waves are unique to GI muscle• Intensity usually varies between 5 and 15 mv• Frequency ranges in different parts of the human GIT from 3 to 12 /min• Cause • Complex interactions among the smooth muscle cells and
specialized cells Interstitial cells of Cajal - pacemaker cells
Spike Potentials
• True action potentials- Occur when slow waves reach threshold- Cause SM contraction
• Frequency- Affected by nervous / hormonal stimuli- frequency stronger contraction
Figure 62-3; Guyton & Hall
Each time the peaks of the slow waves temporarily become more positive than -40 millivolts, spike potentials appear on these peaks
The higher the slow wave potential rises, the greater the frequency of the spike potentials, usually ranging between 1 and 10 spikes per second.
AP of the gastrointestinal smooth muscle
• Channels responsible for the AP allow large numbers of calcium ions to enter along with smaller numbers of sodium ions and therefore are called calcium-sodium channel
• These are much slower to open and close than are the rapid Na+ channels of large nerve fibers
• Accounts for the long duration of the action potentials
Changes in Voltage of the R M P
• Resting MP averages about -56 millivolts• Multiple factors can change this level• Factors that depolarize the –excitable—– Stretching of the muscle– Stimulation by acetylcholine– Stimulation by parasympathetic nerves that
secrete acetylcholine– Stimulation by several specific gastrointestinal
hormones.
• Important factors that make the membrane potential more negative—hyperpolarize the membrane and make the muscle fibers less excitable—– Effect of norepinephrine or epinephrine on the
fiber membrane – Stimulation of the sympathetic nerves that secrete
mainly norepinephrine at their endings
Calcium Ions and Muscle Contraction
• Occurs in response to entry of calcium ions• Calcium ions, acting through a calmodulin control
mechanisms
Neural Control of GI Tract
• Intrinsic Control - Enteric nervous system
- Myenteric (Auerbach’s) plexus- Submucosal (Meissner’s) plexus
• Extrinsic Control - Autonomic nervous system- Parasympathetic - mainly stimulates (Ach) - Sympathetic - mainly inhibits (NE)
Physiological anatomy of enteric nervous system
Enteric Nervous System (ENS)• Location - gut wall from esophagus to anus
ENS - Myenteric Plexus
• Location -- Esophagus to anus- Between longitudinal and circular SM layers
• Function - controls GI motility- Stimulatory influences -
• tonic contraction (tone) • contraction frequency / intensity (propulsion)
- Inhibitory influences• Decreased Sphincter tone (relax) - pyloric sphincter,
ileocecal sphincter, LES
Figure 62-4; Guyton & Hall
ENS - Submucosal Plexus• Location - Mucosal layer from esophagus to
anus• Function - Local control
- Secretion- Absorption- Contraction of muscularis mucosa
Parasympathetic Innervation• Cranial Division - (Vagus N.) - first half of gut
• Sacral Division - (Pelvic N.) - second half of gut
• Neurons - preganglionic - long
- postganglionic - short, entirely in ENS
Synapse with ENS neurons (mainly)
• Stimulation - Excites ENS (in general)
Sympathetic Innervation• Preganglionic Neurons- Originate at T5-L2 (cell bodies)
• Postganglionic Neurons (long)- Originate in ganglia - Innervate entire gut
• stimulation of the sympathetic nervous system inhibits activity of the gastrointestinal tract causing many effects opposite to those of the parasympathetic system• Direct effect of secreted norepinephrine to inhibit intestinal tract smooth
Muscle• Inhibitory effect of norepinephrine on the neurons of the entire enteric
nervous system
Organ Effect of Sympathetic Stimulation
Effect of Parasympathetic Stimulation
GutLumenSphincter
Decreased peristalsis and toneIncreased tone (most times)
Increased peristalsis and toneRelaxed (most times)
Neurotransmitters • Preganglionic efferent neurons - acetylcholine
• Postganglionic efferent neurons - PNS - acetylcholine- SNS - norepinephrine
• Enteric nervous system (many others)- Excitatory - acetylcholine, substance P- Inhibitory - VIP, NO
Sensory Afferent Neurons
• Stimulation of afferent neurons- Distention of gut wall- Non-specific irritation of gut mucosa- chemical stimuli
• Stimulation - can excite or inhibit- Intestinal movements- Intestinal secretions
Figure 62-4; Guyton & Hall
Gastrointestinal Reflexes
• Reflexes that are integrated entirely within the gut wall enteric nervous system– Control GI secretion, peristalsis, mixing contractions
• Reflexes from the gut to the prevertebral sympathetic ganglia and then back to the gastrointestinal tract– Gastrocolic reflex– Enterogastric reflexes– Colonoileal reflex
• Reflexes from the gut to the spinal cord or brain stem and then back to the gastrointestinal tract– Reflexes from the stomach and duodenum to the
brain stem and back to the stomach– Pain reflexes that cause general inhibition of the
entire gastrointestinal tract– Defecation reflexes
Thank you