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 Slow waves are unique to GI muscle 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 Frequency Occur when slow waves reach threshold Cause SM contraction Frequency Affected by nervous / hormonal stimuli frequency stronger contraction
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. Figure 62-3; Guyton & Hall
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
Function - controls GI motility 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 Gut Lumen Sphincter Decreased peristalsis and tone Increased tone (most times) Increased peristalsis and tone Relaxed (most times)
Neurotransmitters Postganglionic efferent neurons 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
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