Cardiac Muscle Notes

Cardiac muscle -striated

-myogenic- initiate contractions itself, doesn’t require nervous stimulation but its activity can be modulated by nervous impulses from the ANS

Structure

-cells are uninucleate, centrally placed nuclei and are connected to each other by intercelated disks (seen as dark lines on a light microscope) arranged in layers- laminae which are branched and iterdigitate

Intercalated zones:

-main type of membrane to membrane contact is fascia adherens- the actin filaments at the ends of the terminal sarcomeres insert into anchor proteins, catenins/vinculin/alpha actinin which also bind to transmembrane proteins cadherins- these spand the plasma membranes and bind to identical cadherins on adjacent cells. Light microscopy, zona adherens can be seen as a small electron dense plaque on the cytoplasmic side of the plasma membrane fasciae adherns and transmit contractile forces

-Desmosomes: provide anchorage for the intermediate filament

-The adhering junctions allows transmission of mechanical forces- cadherins are transmembrane proteins, overlapping segments of the cadherin molecules bind to anchoring proteins desmoplakin

-Z lines, ruffled cell membranes abut each other to form intercalated disks-

-intercalated discs contain gap junctions (Cx43)- allow for the spread of electrical excitation between neighbouring fibres gap junctions allow the heart to function as a 3D synctium

-T Tubule system is present

-straited muscle- sarcomeric arrangement

-Between muscle fibres are collagenous tissue with rich capillary network

-Heterogenous organ- myocytes adapated for different purposes in different regions of the heart, some cells involved in contraction, conduction, pacemaking- SA node, AV node, fast conduction system: HIS bundle, purkinje fibre, atrial and ventricular myocytes

-atrial and ventricular myocytes specialisied for contraction so are much bigger cells and are packed with myofibres.

Function of the heart

-muscular pump that pumps blood around the body

-nervous system alters the force and rate of heart beats

Excitation: contraction is not iniated by neurons but by electrical excitation originating the heart’s pacemaker. Cardiac muscle receives synaptic input from the autonomic neurons which is used to modulate the heart rate

Spread of impulse through the heart

-SA node, a specialised knot of myocytes in the right atrium that generate an action potential rhythmically – SA node- pacemaker

-Due to the presence of Gap junctions, the impulse is propagated through the atria where it triggers atrial contraction

-the atria are separated from the ventricles by a non conducting fibrous ring of tissue- atrioventricular septum- excitation can only spread into the ventricle at the AVN

- conduction through the AV node is slow, ensures the atria contract fully before the ventricles contract

-after a 100ms delay, conduction is fast through the HIS and purkinje fibres. From the purkinje fibres action potential is conducted from the base to the top of the ventricles- allows for synchronous activation of contraction in the ventricles

Action potentials

-As the heart is a heterogenous organ, the myocytes in specific regions of the heart have different functions which mean they are specialised by having a distint set of ion channels

-the ion channels found in different regions of the heart are regulated in different ways

-Due to this the the intiation time, duration and shape of an action potential that occurs in the different regions of the heart varies according to the cell type

ACTION POTENTIAL IN THE Sino Atrial Node

-SAN – spontaneous depolarisations-generating action potentials- determines the rate of the heart beat- always draw the graph

-maximum diastolic potential is -60mv ,less negative than in ventricular cells- this is due to large background Na current through background sodium channels (not voltage gated)- always open- Na influx due to the large electrical gradient

-No inward rectifying potassium channels I_k1, SAN cells lack the background potassium efflux to stabalise the Em so there is a progressive increase in Em from -65mv to -40mv, then an action potential is initiated

-the rising Em is due to the pacemaker current-NET inward current

-De-activation of voltage gated delayed rectifier K channels (rapid, I_Kr) + slow (I_Ks)

-rising Em during diastole is first due to the background Na current-causing the membrane potential to rise

-then there is the activation of hyperpolarisation activated cyclic nucleotide gated channels HCN4 –Voltage dependent channels- these channels have a Nernst reversal potential of -20mv as they are equally permeable to both sodium and potassium- this causes the membrane potential to be further depolarised- open and close slowly and are cAMP regulated- more activated during sympathetic innervations- prepotential slope steeper

Evidence: When a membrane permeable analogue of cAMP is added to an HCN channel that is excised there is an increase in current measured by voltage clamp. To show that the activity is not increased due to protein kinase A, the enzyme is blocked

-this then leads to the activation of T type voltage gated calcium ion channels towards the end of the pacemaker depolarisation-which leads to influx of calcium ions- Voltage dependent inactivation- so open for a short period of time- small current, pulsatile activity- the conductance is low

-activation of an inward current due to Na-Ca exchanger – 1 calcium out, 3 Na+ in, activated by calcium which binds to allosteric site.

-neurotransmitters modulate the currents determing the slope of phase 4 depolarisations

Upstroke of action potential

-when the SAN cells reach threshold, action potential is triggered

-opening of L type voltage gated calcium ion channels- nodal AP propagates slowly as it is driven by weak calcium influx during AP upstroke. Evidence- no action potential is generated if the calcium channels are blocked by verapamil- used as a drug for hypertension These cells have no...

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