Smooth Muscle Physiology Flashcards
What are the differences of skeletal cardiac and smooth muscle by type
Skeletal - straited and voluntary (somatic innervation by a and y motor neurons)
Cardaic - straited and involuntary
Smooth - untraited and involuntary
autonomic intervation (sympathetic and parasymapethic postganglionic fibres)
what is the differences of skeletal cardiac and smooth muscle by individual muscle fibres
Skeletal - large elgoanted cylindrical and possess multiple nuclei
Cardiac - large cylindrical and poss multiple nuclei
Smooth - small spindle shaped and posses one nucleuis
What does straited mean
what does voulntary and involuntary mean
straited means it contains scaramoeres
voluntary means you can control it will involuntary means it does it rest and digest and fight or flight
Function of Smooth Musucle in different locations
Vasculature
Airways
Urinary System
Vasculature - controls diameter regulated flow and pressure
Airways - controls diameter regualted flow and resistance
Urinary - propulsion of urine into ureters bladder tone tone of internal sphincter of bladder
Function of Smooth Musucle in different locations
Reproductive tract
Gatrintestinal tract
Skin
Male - secretion of sement
Female - proulsion of egg in fallopian tubes partiution in uterues
Skin - Pili erection
What is the difference in shape and function of smooth muscle in the artery bronchiole and colon
Artery - arrned cyclindrial around the arteries contract and relax for blood pressure
Bronchole - small airways of lungs with muscle allow reduce increase bore of airways increase partial pressure more surface area
Colon - medtaite repulsive movement some curvature
What is Multiunit smooth muscle
Allow
Word
how they function
example
electrical isolation of cells allows finer motor control
Tonic
Function individually
Iris and vas feernes
What is Unitary
Permit
Function
Example
Word
gAP JUNCTIONS PERMIT COORDINATED CONTRACTION
function as a syncytium
stomach urinary bladder and bronchioles
Phasic
What does Tonic and Phasic
Phasic constanltu engaged which provides a level of contraction (tone)
Tonic - slightly more contraction when stimulated controlling movements
Function of relaxation to contracted
Contrctile arhcolines to a cytoplasm in the cell membrane (dense bodies) rather than the structural protein
Net like structure muscle cross bridges are formed sliding mechanism is ended pulled relaxed and contracted
Xontractile machinery of Smooth Muscle
relies on sliding filament mechanism of generated during actin myosin cross bridge formation to facilitate contraction
Cross bridge formation and sliding filament in smooth muscle
- driven by a rise in CA which binds to calmodulin
- Ca calmodulin complex actovayes myosin light chain kinase
- Myosin light chiaan is phospahted on the myosin head
- Phosphoylation of myosin head ‘cock’s it and increases its ATPase activity reading it to interact with actin to form a cross bridge
Factors (2) affecting straited muscle cross bridge formation
CAS
incresed intraceullar Ca
stretch (Frank Sarling relationship)
Factors affecting smooth msucle cross bridge formation (3)
CIP
Increase intracellular Ca
Phophylation of myosin light chain kinase
Inhibition of myosin light chain phopahtase
What is calmodulin
Mulifunctional Ca2+ binding protien present in the cytoplasm of all eykarytoic cells
Ca can affect the protein and changes the light chain kinase
Calmodulin - Ca calmodium - CaM associated with a CaM kinase
What does relaxation of smooth involve
Drop in Ca and Depohoyrlation
How does Ca return to preexcitation cocentrations
Membrane bound Ca ATPase and Na Ca exchanges exepl calcium from the cell and calcium is sequestered into stores by sarco (endoplasmic reticulum calcium) ATPase (SERCA)
How does depohosylation occur
Myosin light chain phopahtase
How is innervation by autonomic nverous system in:
Aterial smooth muscle
Other smooth muscle
other point
Aterial - symapethic with noradrenaline
Other - both para and symapethic with acetylcholine
vast networks of nerual supply
What is Parhamoechical coupling
process which agent causes a chnage in smooth muscle without change in membrane potential
involved production of intraceullar second messengers that wither contract or relax
what is Parhmoemchaical coupling important second messerngers
IP3 cuasinc contraction
cGMP and cAMP cuasing relaxtion
what is electrochemical coupling
opening of plasma membrane voltage actiavted L type Ca channels in response to depolarisation with or without action potential generation
Steps for Pharmocochemical coupling
Hormone Binds to GPCR
Phophildase PIP2 -> IP3 + DAG
DAG causes PKC activation CP17 decreases MLCK in myosin head
actives activity of MLCK no action potential
steps for phasmochemical coupling
Calicum binds to Sarplasmic
Ca exits cytoplasmi inudes release activation of myosin cross bride contractionaction optential opening L type calcium channels
Steps for restoring Ca
Sodium Ca cell membrane uses electrochemical graident sodium inside is low
Calcium out extracellular Ca ATPase ATP
Regulation of smooth muscle tone receptors
Regulation of Smooth muscle tone uses L type Ca channels and GPCR Gq to bring Ca into the cell
Regulation of smooth muscle tone binding
The ca binds to the calmodulin to form a Ca Calmodulin complex that makes MLCK Active
Regulation of smooth muscle tone contraction
Active MLCK phosphorylates MLC which causes a contraction
Regulation of smooth muscle tone relaxation
Cyclic GMP actives PKG which makes MLCP active
Active MLCP dephorylates MLC which causes relaxation
NO moving into the smooth muscle cell
Organ Nitrates from tissues comes into the smooth muscle cell from endothelial cell
Endothelium dependent vasodialtion relaxation
NO activates guanylate cyclase which breaks down GTP to cGMP causing the activation of Protien Kinase G causing relaxation
Endothelial making NO citrulline
the vasodilating substances increase the Ca in the endothelial cell which binds to calmodulin and this complex Ca calmodulin complex activates eNOS which actives L arginine + O2 to form No + citrulline which goes into the smooth muscle cell
how does PKG cause relaxation
PKG can increase activity of membrane bound potassium channels. the channels respond to voltage membrane potential which reduces calmodulin complex and reduces MLK causing relaxation
PKg stimulates and actives
PKG stimulates MLCP , PMCA , SERCA and activates K+ channels that cause hyperpolarisation and inactive Ca channels
what is angina
Angia means that there is no sufficent supply of blood the myocardium with oxygen
Agina is caused fixed vessel narrowing and endothelial dysfunction
stable vs unstable angina
stable angina is episodic brought on by exertion relieved by rest and unstable angina is symptomatic even at rest
NO production and relaxation
Organic Nitrates act directly on the smooth muscle cell to increase NO production. same signalling cascade as endogenous NO release leads to smooth muscle relaxation and therefore vasodilation
action and where of NO
Acts primarily on veins to reduce preload and oxygen demand in the myocardium. secondary action on the coronary collaterals to improve oxygen delivery to the ischaemic myocardium
Relief of NO
this system gets relief given fast acting or can also get a longer working one reduce symptoms and exploits NO in the skeletal muscle cell
Effects of organic nitrates on Venodilation:
Effects of organic nitrates on Venodilation:
this primary action of organic nitrates is to induce venodilation
venodilation reduces venous pressure and the venous return to the heart
this reduces work of the heart
reduces oxygen demand
effect of organic nitrates on the coronary collaterals diagram
when there is atheromatous plaque means there is less blood flow to the ischaemic myocardium however organic nitrate dilates the collateral which means both sides are even
Glyceryl Trinitrate
Glyceryl Trinitrate - do no directly release NO biologically inactive, have a half-life of 40 mins and have a low bioavailability
Isosorbide Dinitrate
Isosorbide Dinitrate - do no directly release NO , biologically inactive , half life of 2 - 4 hours and bioavailability varies
conditions managed by phasrmacological manipulation of smooth muscle consequences
conditions managed by phasrmacological manipulation of smooth muscle consequences include left ventricular hypertrophy , renal failure , stroke
Calicum blockers act on what
Calcium channel blockers act at L type calcium channels on vascular smooth muscle but also at l type calcium channels in cardiac myocytes
three main classes of calcium channels blockers
the three classes of calcium channels blockers: dihydropridines , benzothiazepines and phenylalkylamines
what do KATP channel openers cause
K channel openers in serve hypertension can be used with beta blocker and diuretics and opens KATP channels in the smooth muscle cell membrane and hyperpolarise the smooth muscle cell
a blockers
a1 adrenoreceptors are the first part of the signalling cascade that ultimately leads to smooth muscle contraction following activation of sympathetic nervous system leading to vasodilation
