HSF 2 - Unit 2 Physiology: Smooth Muscle Flashcards
(27 cards)
what different parts of the body have smooth muscle?
vasculature, airways, gut
what is a multi-unit? how does it function?
electrical isolation of cells allows finer motor control; each one contacted and innervated by a separate axon and work as separate units; ex: ciliary muscles of the eye, each behave independently
what is a single unit? how does it function?
gap junctions permit coordinated contraction, work as a single unit; a single nerve fiber axon comes and branches to connect to different cells; ex: visceral smooth muscle; organs, airways, uterus, coordinated
what is the structure of smooth muscle?
smaller than skeletal muscle, single nucleated, not organized in tight sarcomeres so no striations, still use actin and myosin, contraction speed is slower, contraction time is longer due to SR calcium pump
what is the membrane potential of smooth muscle?
-50 to -60 mV
what are the different membrane potentials in smooth muscle?
spike, plateau, slow waves
what is an example of each type of smooth muscle-action potentials?
spike: VGCC in the intestinal wall
plateau: uterus VGCC
slow waves: intestinal wall leaky calcium channels; repetitive spikes are self excitatory (pacemaker potentials)
what are the different generators of the action potentials?
electrical stimulation, action of hormones, transmitter substances, stretch, spontaneous generation
why are plateau action potentials shaped in the way they are?
they have a slower depolarization rate compared to sodium channels, slow depletion of calcium from the cell
what are the 5 ways in which calcium can enter the cell and have various effects?
1) through caveoli VGCC
2) stretching and calcium channels open
3) NT and hormonal receptors
4) CICR
5) SOCE
CICR
calcium induced calcium release, respond when there is increased calcium intracellularly and release calcium from the SR to further raise intracellular calcium levels
how does the intracellular messenger pathway with neurotransmitter/hormonal receptors work?
receptors are coupled with a G-protein and activate the complex, which then activates PLC to cause formation of IP3 from PIP2, and DAG is released; IP3 activates the SR IP3 receptor which causes calcium to be released from the SR
SOCE
store operated calcium entry; with the store being SR; STIM1 is on the SR and when it runs out of calcium it sends a message to the ORI1, which is located on the plasma membrane, to let more extracellular Ca in so SR can be restocked
how does smooth muscle contract?
increase in intracellular calcium; calcium binds to calmodulin, Ca/Cam binds with myosin light chain kinase (MLCK) and this phosphorylates the myosin light chain (active form); crossbridge cycling can occur
how does smooth muscle relax?
can change contraction by altering levels of Ca and myosin and phosphatase activity; for relaxation needs low Ca and increased phosphatase; if no phosphate, detaches the myosin from the actin; release of nitric oxide by the endothelium causes smooth muscle relaxation, decrease in NO can be a sign of vascular disease
what is the process of endothelium in vascular smooth muscle relaxation
ACh comes and activates MR, which causes downstream PLC and IP3 activation and thus calcium to bind to calmodulin, this activates eNOS (synthase for NO) to make NO from arginine, this activates guanylyl cyclas to make cGMP from GTP and causes muscle relaxation since cGMP inhibits Ca entry and activates MLC phosphatase
how does viagra result in vasodilation?
inhibits the degradation of cGMP to GMP by inhibiting the phosphodiesterase that does this and inhibits Ca entry by activating MLC phosphatase by activation og PKC
what are the cholinergic receptors?
muscarinic and nicotinic: M1-M5 (M3 in SM)
what are the adrenergic receptors?
alpha 1, alpha 2, beta 1, beta 2 (catecholamines)
what happens in result of the release of NE? (alpha)
alpha 1 receptors: Gq - PLC - IP3 - increased Ca; results in more myosin and actin interaction and thus more contraction of smooth muscle (vasoconstriction)
what happens in result of release of Epi or NE? (beta)
beta 2 receptors: Gs - adenylate cyclase - cAMP - leads to inhibition of MLCK; decrease in myosin and actin interaction thus decreased contraction of smooth muscle (vasodilation)
there are receptors for ACh on … what happens in each instance?
both endothelium and smooth muscle; ACh releases NO from endothelium or can cause smooth muscle contraction directly; get vasodilation from NO
what happens to the beta 2 receptors when there is more Epi than NE?
Gs - adenylate cyclase - cAMP - PKA - closes Ca++ channels; decrease myosin and actin interaction, decreased contraction of smooth muscle (bronchodilation)
what does ACh stimulate in muscarinic receptors in bronchioles?
Gq - PLC - increased cytosolic Ca++
increase smooth muscle contraction (bronchoconstriction)