general function is to move contents of tubes/ organs
(via contraction/ change in diameter)
- spindle shaped
-no striation / parallel sarcomeres
Smooth compared to Skeletal
SIMILAR: Length Tension relationship, Max. tension per unit cross sectional area, in both oxidative fibers weaker than glycolytic
DIFFERENT: Smooth can develop tension over larger range of lengths[these muscles are constantly stretching to fill and contracting to release],
(however as a single cell, smooth can develop less absolute force)
Smooth Muscle Thick/ Thin filaments:
one of the Myosin Light Chains on the neck of the thick filament is the site of contraction regulation
How is Smooth Muscle Contraction Activated by Ca2+
regulated by cytosolic Calcium (like in skeletal) but action of Ca2+ is more sig.
^Ca2+ , binds to protein Calmodulin, Activation of Ca-cal. myosin light chain kinase: phosphorylation of MLC, cross bridge cycling
ATP utilization: lower than skeletal muscle
shortening velocity is slower ^
Cross Bridge Cycle (Smooth) [tension n shortening]
other than the attatchment step: same as Skeletal
The energized cross bridge (with ADP +PO4 bound to head) interacts with actin- power stroke occurs( due to release of PO4 and ADP )> ATP binds to detach the cross bridge > hydrolysis of ATP re-energizes the head and crossbridge cycling can occur again, AS LONG AS THE PO4 IS STILL BOUND TO THE MLC.
Ca2+ levels decrease: less MLCK active: MLC phosphatase dominates (dephosphorylated
How is Ca2+ removed from the cytosol
ATPase on plasma membrane
Ca2+- Na+ exchanger on the plasma membrane (Na+ gradient is energy source)
ATPase on SR membrane
Calcium into Smooth Muscle:
can come from ECF (calcium channels on plasma membrane) or SR (calcium channels on this membrane: opened by second messengers)
Signals for Activating Smooth Muscle
*one input: the Motor neuron (release of ACh is always excitatory (cause of contraction) )
>>> Membrane depolarization: AP may be generated, but not necessary.
>>> Chem. Messangers (such as Hormones, Paracrine Factors, Neurotransmitters, and Local Metabolites): can excite or inhibit
>>> Stretch: mechanical changes may cause Ca2+ channels to open: causing contraction.
Smooth Muscle Activation and Inhibition
1. A change in membrane potential will initiate Contraction by Opening of V-gated Ca2+ channel on the plasma membrane.
2. ligand gated Ca2+ channels: G-protein activated by messenger molecule to membrane receptor> opening or closing of these channels = mediated
Smooth Muscle Activation/ Inhibition continued
3. Opening of Ca2+ channels on SR without AP:Binding of a messenger molecule to a membrane receptor activates a G-protein mediated 2nd messenger cascade that generates IP3 and IP3 will gate the SR Ca2+ channel open.
4. Stretch activated channels: (contraction to oppose the stretch) Alternately, decreased stretch will close these channels and lead to relaxation of the fibers.
smooth muscle cells do not utilize V-gated Na+ and K+ channels to generate AP
Depolarization is due to Ca2+ influx!
*slower rate of Dep. and Rep. has a lower peak amp.
A:Ca2+ dependant K+ channels close and the membrane depolarizes B:Voltage-gated Ca2+ channels open and AP occurs, cytosolic Ca2+ rises C: Ca2+ dependant K+ channels open and membrane hyperpolarizes D:V-gated Ca2+ channels close and cytosolic Ca2+ decreases
Closer look at the Pacemaker Steps : A
Originally @ most hyperpolarized state, Ca2+ dependent K+ channels close, membrane depolarization due to decreased K+ efflux
Closer look at the Pacemaker Steps : B
Depolarization to threshold opens Ca2+ channels. Ca2+ levels in cytosol increase
Closer look at the Pacemaker Steps : C
Ca2+ interacts with Ca2+ dependent K+ channels which reopen. Membrane repolarizes (hyperpolarizes)
Closer look at the Pacemaker Steps: D
Ca2+ channels close/ cytosolic Ca2+ levels decrease leading back to step A
Connected to nearby/adjacent non-pacemaker smooth muscle cells by Gap Junctions
WHICH aid in speed, increase cell synchronization, are bi=directional...
Single Unit Smooth Muscle
1.Contain pacemaker cells
2.Connected by gap junctions
4.Activity altered by inputs (ie. autonomic innervation near/ circulating hormones/ paracrine factors) to pacemaker cells
5.Contraction can be initiated by stretch
---Examples:GI, uterine and small diameter blood vessel smooth muscle.
Multiunit Smooth Muscle
*individual cells are separate from each other...
Few or no gap junctions 1.Activity is not synchronous- APs not utilized to generate force
2.No pacemaker cells
3.(Autonomic neurons= extensive)Richly innervated throughout the muscle
4.Not responsive to stretch
5.Contractions often do not require AP’s in the membrane
6.Examples:Airway and large artery smooth muscle
for molecule transport over large distances (between in and external environments)
extracellular fluid: plasma and interstitial fluid
*murmurs are not usually an issue if there is no significant change in stroke volume.
Diagnosing a murmur
heard during systole: (right after 1st sound)
Aortic/ Pulmonary Stenosis, AV valve Insufficiency
heard during diastole: (right after 2nd sound)
Aortic/Pulmonary Insufficiency, AV Stenosis
Regulation of Heart Rate and Stroke Volume
CO <Liters per minute produced> = SV<determined by force contraction of ventricle> x HR <determined by rate of SA node>
^direct influence on one another.
Autonomic Innervation of the <3
Vagus nerve (PARASYMPATHETIC): stimulates SA and AV nodes *specifically to pacemakers (?) ---------effects Heart Rate (opposite) :: ^ para, decrease HR
SYMPATHETIC cardiac nerve: stimulates SA and AV node, and Ventricular myocardium(muscle) ----------effects both Heart Rate and Stroke Volume (directly)
Autonomic Innervation Simplified!
Parasympathetic activity releases ACh, and thus reduces Heart Rate
Sympathetic activity releases Nor-Epi, and thus increases Heart Rate
ANOTHERRR look at the Autonomic Innervation
Control of HR: via changes in
1. symp. activity (increases permeability to Na and Ca> more influx)
2. parasymp. activity (increased permeability to K > more efflux) (also reduces permeability for Na and Ca)
3. Circulating Epinephrine levels
Control of SV via
1. Changes in symp. activity (increases contractility)>> expression of beta adrenergic receptors
2. The Frank-Starling Mechanism (Starling's Law of the Heart)
(shows us that ^ symp. activity, no matter the EDV, ^ contractility):: ^EF
Symp activity.. increases contractility.. contraction occurs with more force.. End Systolic Volume change (from End Diastolic Volume) is greater, Stroke Volume ^
EF=SV/EDV : aka. with increased contractility, EF increases.
Another look at Symp. Activity Effect on Force Contraction
3 things different between the two ventricular muscle twitch tracings
-shorter rate of contraction (duration) (b/c of Nor Epi.) -faster rate of relaxation (b/c of ^ Ca2+ removal, and lowered affinity of troponin for Ca2+) -greater peak tension (b/c of cytosolic Ca2+ increase-- more open channels)
Effect of Epi/ Norepi on Ventricular Muscle Cell
Activates cAMP- dependent protein kinase
- Ca2+ channels Open> more Ca2+
- Increases cross-bridge cycling
- Increases rate of ATPase activity
Overall Effect of Increasing HR
More blood in systole, less in Diastole (less fill)
under sympathetic activity, contraction and relaxation is completed more quickly to allow for more filling time
Frank Starling's Law of the Heart
(different mechanism to alter SV... not about contractility)
*** this is like the basic curve, not looking at the effect of symp. activity.
What this says is that an increased EDV (fill), leads to an increased Stroke volume
thus: ^ symp. activity :: decreased VR:: ^ cardiac filling, and CO
LAW: ^ EDV = ^SV
Cardiac Muscle Length-Tension Relationship
Stretching of cardiac fibers ^ the amt of tension generated
(stretch of ventricles during fill results in a more forceful ejection of blood)
^ cardiac fiber length = ^ tension
(to a point!! (optimal level)
•SV^ as EDV^
•At any given HR, an increase in VR* will increase CO
–Increased VR → increased EDV → increased stretch of cardiac fibers → increased force of contraction → increased SV → increased CO
How can VR be altered?
change venous pressure
(either by ^ PVP or decreasing CVP, or the Addition of volume of fluid/ constriction of veins)
constricted Arterioles (higher resistance)=higher MAP (fluid backup!), decreased cap pressure
*like a hose*> pressure drives flow
Major controller of TPR = changes in/ of Radius
ARTERIOLES PROVIDE MORE THAN 1/2 the TPR
Vasoconstriction (^ arteriorlar R, ^ MAP and decreased Pcap) Vasodilation (decreased arteriolar R, decreased MAP and ^ Pcap)
Radius is controlled by hormonal input, paracrine factors, sympathetic neural input, and changes in local metabolites)
How can Hormones (aka. Epinephrine) act as both vasoconstrictors and vasodilators?
Different tissues have different epi Receptors!
alpha receptor: constrict (most tissue)
beta receptor: (usual response) dilation (at least in low/ moderate epi amounts)
- example^ exercise
the rule of thumb we go with though is symp activity causes constriction
Types of movement across capillary wall
Diffusion (MOST IMPORTANT MEANS OF NET MOVEMENT OF NUTRIENTS...)
^O2 and glucose from blood to muscle, CO2 out!^
UltraFiltration (bulk flow driven by pressure diff)
(opposite= (re)absorption)^from plasma to interstitial fluid^
aka Outward movement; net filt occurs at arterial end, wile net absorb (inward movement) occurs at venous end
Exocytosis/Endocytosis (moves specific proteins)
daily fluid movement across caps
Ultrafiltration: 20 L/ day
Osmotic reabsorption: 17 L/ day
Lymph: 3 L/day (another form of returning ISF to plasma
Edema (swelling associated w. increased ISF volume)
(^ ultrafiltration) due to ^ in Pcap
Disruption of lymph flow
Arterial Pressure is Homeostatically Regulated
MAP drives flow, and must be maintained to ensure adequate O2/nutrient delivery... and removal of CO2/ metabolic end products
Receptors/sensors are the Arterial baroreceptors (carotid sinus and aortic arch)
MAP ^= Firing Rate ^... etc
effector tissues are conducting system (HR), cardiac muscle (SV) and blood vessel smooth muscle (TPR and VR)
Decreased blood volume causes:
decreased: VR, SV and CO
Arterial constriction (to increase the decreased Arterial pressure, and to decrease the capillary pressure)
*autotransfusion* reabsorbtion into caps to make up for lost fluids (dilute) (decreases ultrafiltration)
diversion of blood flow to maintain perfusion to heart and brain
via local controls: not via altered symp/ circulating epi... resistance doesn't change due to the hemmorage
but a Baroreceptor reflex (plays major role in blood pressure regulation in various situations)>
constriction on arterioles: and increased resistance to tissues. due to increased sympathetic and epi.
In the case of heart attack: what does a baroreceptor reflex do?
Immediate responses (not baro)
Decreased SV (CO)
VR increase/ increased contractility
SV, CO and MAP increase (but not to normal)
Heart Failure (inadequate CO)
>> can be due to systolic (pump) fcn [cause: <3 attack/ arrhythmia]
or diastolic (fill) dysfunction [cause: hypertension]
chronically increased systemic arterial pressure
caused by ^TPR
Increases the afterload (pressure in arteries) on the <3
---- problem with this: high arterial pressure means ventricles musc contract w. more force, thus ventricular walls get thicker [hypertrophy]... WHICH CANNNN: decrease chamber size :( ((decreased EDV) (decreased SV...))
Coronary Artery Disease
insufficient blood flow to an area of <3 muscle (often caused by plaque in vessel wall/ narrowed lumen)
<3 attack can be caused by ruptured plaque/ formation of clot OR lodging of an embolism
Inadequate SV> inadequate CO> inadequate MAP> inadequate perfusion of tissues> kidney/liver damage or failure, high risk of heart attack, stroke and sudden death
If LV pumps less Forcefully than RV???
fluid backup in lungs! P^ (edema??)
^ CO, HR, SV, MAP, and lower TPR (due to vasodilation)
*MAP can be up bc of the elevated CO
Skeletal and Respiratory pumps aid in maintaining venous return (cardiac output) during exercise
** venous tone ^ due to ^ symp stimulation
control of CV system: increase of MAP by resetting Baroreceptor set point
Effect of Training:
On HR: decreased at rest and exercise, but no change in MAX rate
On SV: increased at rest and exercise due to moderate hypertrophy and increased chamber size (^ strength of contraction)
On CO: ^ MAX, no change @ rest
On Vo2 Max:^ with training (b/c of CO increase)
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