Regulation of GI function: Nerves and Smooth Muscle Flashcards
syncytium
muscle fibers of gut are electrically connected through large numbers of gap junctions
- thus AP spreads throughout all neighboring fibers
Slow waves
GI contractions occur rhythmically, this rhythm is determined by frequency of “slow waves”
- slow undulating changes int eh resting membrane potential
interstitial cells of Cajal
slow wave cells that act as electrical pacemakers for smooth muscle cells
- undergo cyclic changes in membrane potential due to unique ion channels
spike potentials
true action potentials
occur on top of slow waves, when Vm is more positive than -40 mV
channels responsible for APs?
calcium-sodium channels
- much slower to open and close than rapid Na+ channels
Factors that depolarize the membrane and make it more excitable?
- stretching of muscle
- stimulation by ACh released from PS nerves
- stimulation by several GI hormones
important factors that hyperpolarize membrane? make it less excitable?
- NE/ Epi
2. stimulation of sympathetic nn.
how does smooth muscle contracts
entry of Ca2+ ions
- slow waves only cause influx of Na+, thus don’t cause muscle contraction. The spike potentials result in the Ca2+ entering fibers
tonic contraction of smooth muscle
continuous, not associated with slow waves
caused by continuous repetitive spike peotentials or by hormones that bring about partial depolarization
can also be caused by continuous entry of Ca2+
enteric nervous system
GI tract Nervous system
-lies entirely in wall of gut from esophagus to anus
two plexuses of ENS?
myenteric/auerbach’s plexus: outer plexus b/w longitudinal and circular muscle layers. controls GI mvmts
inner/Meissner’s plexus: lies in submucosa. controls Gi secretion and bloodflow
Myenteric plexus
controls GI mvmt: lies within the muscle
- increased tonic contraction of gut wall
- increased intensity of contractions
- increased rate of rhythm of contraction
- increased velocity of peristaltic waves
VIP is inhibitory to this plexus
Submucosal plexus
controls GI secretion and bloodflow
ACh
excites GI activity
secreted via vagus nn.
cranial and sacral plexuses
postganglionic neurons
of GI PS are located in myenteric and submucosal plexuses
Sympathetic fibers
inhibit GI tract activity
originate at T5-L2
Multi-unit SM
one fiber –> one SM
for “fine tuning”
little or no gap junctions
Single-unit SM
one fiber/nerve –> multiple cells
coord. via gap jns.
visceral unitary smooth m.
myogenic “pace maker activity” –. slow wave
depolarization APs
spike potentials: opening of slow Ca2+ channels, results in Ca2+ influx
repolarizing
delayed opening of voltage gated K+ channels
K+ efflux
sources of Ca2+ in smooth m?
- voltage gated Ca2+ channels (from outside)
- Sarcoplasmic reticulum (Ca2+-induced Ca2+ release and IP3 Ca2+ channel)
- store operated Ca2+ channel (from outside)
Ca2+ sequestering?
- SERCA of SR
- Ca2+ ATPase pump (sarcolemma)
- 3Na+/Ca2+ antiporter (sarcolemma)
role of Ca2+ in excitation contraction coupling?
in Smooth m. Ca2+ turns on X bridge by inducing chemical change in myosin thick filament via phosphorylation so that it can bind with actin
- skeletal m. induces a PHYSICAL change in thin filament
actin = thin myosin = thick
chemical excitation contraction coupling
CA2+ binds with calmodulin (CaM) which activates myosin light chain complex (MLCK)
- results in conformational change of myosin head and powerstroke via increased ATPase activity
latch state
maintenance of tension in tonic smooth m. without fatigue
