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Flashcards in Smooth Muscle Contraction Deck (34)
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how is smooth muscle different from skeletal muscle in terms of organization?

smooth muscle has thin and thick filaments, but no sarcomere, thus there are no light/dark bands
-thin filaments are anchored to a dense body (cytoskeletal specialization)
smooth muscle doesn't have T-tubules, and has less elaborate SR


how does a smooth muscle twitch differ from skeletal muscle twitch?

slow contraction velocity, slow relaxation, duration of tension is longer
-contract to less than 1/3 of initial resting length (skeletal only 1/4 to 1/3 of stretched length) so can reduce luminal diameter to almost zero



microdomains in smooth muscle sarcolemma that are enriched with various types of cell receptors and ion channels
-in close proximity to SR or mitochondria


speed and force of contraction in smooth muscle

exhibits prolonged tonic contractions lasting hours to days
-X-bridge cycling is slower, but proportion of time spent in tension-generating phase of X-bridge cycle is longer, resulting in greater force of smooth muscle contraction with less E expenditure


temporal relationship of smooth muscle

onset of contraction is slower, and duration of tension is longer in smooth muscle
-AP is Ca++ dependent (unlike Na+ dependent APs of skeletal) meaning inward depolarizing current is carried by Ca++ ions


unitary smooth muscle

(single-unit) electrically coupled via gap junctions (syncytium)
-spontaneously active (like peristalsis), respond to stretch, but not really SNS
-mullions of smooth muscle cells organized in sheets/bundles contract in coordinated fashion as a single unit
-contraction controlled locally


multiunit smooth muscle

made of discrete smooth muscle fibers, each innervated by a single nerve ending
-contraction is seldom spontaneous (need SNS), don't respond to stretch
-electrical isolation of cells allows finer motor control
-contraction controlled neurally


examples of multiunit smooth muscle

airway smooth muscle
piloerector muscle (hair)
ciliary muscle of the eye
some arteriolar muscle (the rest is unitary)


examples of unitary smooth muscle

small blood vessels
GI tract
most arteriolar muscle


sources of Ca++ in smooth muscle

1. influx of Ca++ from L-type Ca++ channels after depolarization of sarcolemma
2. released after agonist binding to GPCR that activate PLC to make IP3
-Ca++ released into sarcoplasm from SR
3. Ca++ induced Ca+ release


can smooth muscle contract without extracellular Ca++?

no, it needs extracellular fluid Ca++, or else inhibited


how is Ca++ removed from sarcoplasm in smooth muscle?

Ca++ pumps in SR and sarcolemma
NCX across sarcolemma
capacitive Ca++ entry


capacitive Ca++ entry

SR is refilled by Ca++ from outside the cell, without triggering AP contraction


how is contraction triggered in smooth muscle?

Ca++ binds to calmodulin on myosin light chain kinase (MLCK), causing phosphorylation of regulatory light chain of myosin
-conformational change in RLC allows myosin to interact with actin


smooth muscle relaxation

myosin light chain phosphatase in sarcoplasm dephosphorylates regulatory light chain of myosin, thus blocking actin-myosin interaction so muscle can relax
-reduction of [Ca++] by Ca++ ion pumps in sarcolemma and in SR membrane can cause relaxation


categories of smooth muscle contraction

electromechanical - AP or stretch cause Ca++ channel opening
pharmomechanical - ligand binding to cell surface receptor
both cause increase in intracellular Ca++ and contraction


spike APs

in unitary smooth muscle; are of short duration relative to contraction time
-depolarization caused by inward current of Ca++ followed by repolarization by outward K+
-initiated by pacemaker (slow) waves


basal electric rhythm
-what is it
-what determines contractile parameters of the stomach as a whole
-what initiates APs

waves of rhythmic depolarization of intestinal smooth muscle cells that originate at a specific point, and are propagated along length of GIT
-pacemaker potentials determine max contraction frequency, propagation velocity, and propagation direction
-APs initiated by release of stimulatory nts from enteric nerve endings


latch state in smooth muscle

extra step from cross-bridge cycle (identical to skeletal)
-during sustained smooth muscle contraction, the Ca++ concentrations in sarcoplasm fall, and myosin light chain becomes dephosphorylated, yet the muscle maintains tension during sustained contractions (still actin-myosin connection)
-not sure how it enters X-bridge again


endothelin formation, release, and what it's stimulated by

ET-1; 21-AA peptide made by vascular endothelium from 39-AA big ET-1 via endothelin-converting enzyme on endothelial cell membrane
-formation and release are stimulated by angiotensin IIand ADH, thrombin, cytokines, ROS, and shearing forces on vascular endothelium


endothelin intracellular mechanisms

once released by endothelial cell, it binds to receptors on target tissue (ET-A and ET-B)
-both coupled to Gq G-PRO and trigger formation of IP3 and Ca++ release by SR for contraction (in vascular smooth muscle and heart muscle)


where ET-A and ET-B are

both are on vascular smooth muscle
-ET-B is on endothelial cells too, stimulating formation of NOS


cardiovascular effects of endothelin

transient vasodilation (initial endothelial ET-B activation) and hypotension, followed by prolonged vasoconstriction and HTN (smooth muscle ET-A/B activation)


diseases/conditions associated with high endothelin

HTN, coronary vasospasm, and heart failure
-ET-1 is released by failing myocardium to contribute to Ca++ overload and hypertrophy
-treat with endotheliin receptor antagonists


alpha-1 receptors in smooth muscle

epinephrine stimulated contraction
-Gq --> PLC --> IP3 --> Ca++ --> calmodulin --> active MLCK --> active myosin-phosphate --> contraction
-in skin arteriolar and gut arteriolar smooth muscle


beta-2 receptors in smooth muscle

epinephrine stimulated relaxation
-Gs --> adenylate cyclase --> cAMP --> PRO kinase A --> inhibits calmodulin --> inactive MLCK-phosphate --> inactive myosin --> relaxation
-in skeletal and heart muscle arteriolar SM, and bronchiolar smooth muscle


phases of local blood flow

1. acute control - rapid changes in local vasodilation/vasoconstriction w/in seconds to minutes
2. long-term control


what happens to blood flow through tissues if availability of O2 to tissues decreases?

blood flow through tissues increases markedly, to try to make up for decreased O2 in blood, maintaining relatively constant supply of O2 to tissues


2 non-exclusive theories for active hyperemia

1. O2 lack theory - low O2 causes smooth muscle relaxation of sphincter
2. vasodilator theory - substances including adenosine are released by active muscle, causing relaxation of sphincter


adenosine for controlling blood flow

controls local blood flow via vasodilation
-minute quantities of adenosine are released from heart muscle cells when coronary blood flow is too little, which causes local vasodilation in heart, but may not be enough on its own


A2 adenosine receptors (2 mechanisms)

relaxation, but NOT adrenergic receptors!
1. A2 couple to Gs --> adenylate cyclase --> cAMP --> PRO kinase A --> calmodulin --> inactive MLCK-phosphate --> inactive myosin --> relaxation
2. A2 couple to ATP-sensitive K+ channels causing smooth muscle hyperpolarization and decrease in Ca++ influx


stress relaxation of smooth muscle

property of biological tissues related to their viscoelastic properties
-increased strain generates stress proportional to change in length
-developed tension remains constant over time
-decline in pressure/stress over time at a constant volume/strain


receptive relaxation of stomach

relax as its volume increases (essential to reservoir function)
-drop in gastric pressure immediately after eating (persists until all solids emptied from stomach)
-vaso-vagal and intrinsic reflexes triggered by activation of mechanosensitive nerve endings in stomach wall
-ACh released by vagal pathways act presynaptically to release more neurotransmitters to actively relax gastric smooth muscle layers, esp. in proximal stomach


action of NO and VIP (vasoactive intestinal peptide) in smooth muscle relaxation

1. NO released by autonomic neuron and endothelial cells
-diffuses to smooth muscle cell, while ACh binds to M3 on endothelial cells, creating more NO
-NO activate guanylyl cyclase and raise cGMP-dependent PRO kinase I cGK1 to elevate MLCP activity to decrease MLC activity
2. with more prolonged/intense stimulation, VIP binds to receptors on smooth muscle cell, and causes delayed relaxation thru increase in cAMP or decrease in Ca++

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