Cellular and Molecular Events in the CVS Flashcards Preview

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Flashcards in Cellular and Molecular Events in the CVS Deck (14):

How is the RMP established

The RMP is set up by the movement of K+ down its concentration gradient created by the Na/K pump, this is because at rest leaky K+ channels are open. Thus, the RMP depends upon the permeability ions and the movement towards their equilibrium potential this causes.


Describe an action potential of a cardiac myocytes.

The RMP is about -85mV and once above the threshold a large depolarisation occurs by the opening of voltage gates Na+ channels. Next there is a transient efflux of K+ beginning the process of polarisation however this stimulates voltage gated Ca2+ channels to open and the movement in of calcium counters the movement of potassium causing a plateau. Once the calcium channels inactivate the cell then polarises as more of the voltage gated potassium channels open.


Describe the action potential at the SAN

The SAN action potential is constantly in cycle the first part of the action potential (the pacemaker potential or funny current If) is due to Na+ (note that the ‘resting’ potential of this action potential is much higher than normal about -60mV). Once above threshold this stimulates the opeing of voltage gated Ca2+ channels which causes a depolarisation, these then close and the cells are polarised again by the opening of voltage gated K+ channels.


Explain why this is a strange action potential?

This is an odd action potential because it is activated at a membrane potential that is less than -50mV. This is because the sodium channels are stimulated not by voltage but are Cyclic Nucleotide gated (full name Hyperpolarisation-activated, Cyclin nuceltide gated channels or HCN).


Why does the action potential start at the SAN even though other parts of the heart has autonomy?

The action potential starts in the SAN as this is the tissue than depolarises the quickest and so overrides the rest.


Which other parts of the heart can establish a contraction of the whole heart?

SAN, AVN and purkinje fibres all have an unstable resting potential and can play a part on pacemaking but only if the ones that are faster i.e. SAN over AVN and AVN over Purkinje are not working.


Describe the cellular structure of cardiac myocytes

Striated muscle with branches and central nucelei. Connected together by intercallated disks. These are where the cells are joined together structurally by desmosones and electrically by gap junctions allowing the flow of ions.


Explain how depolarisation causes calcium release in cardiac myocytes.

Depolarisation of the cell opens L-type Ca2+ channels in the t-Tubule system allowing calcium to move into the cytoplasm. Also localised Ca2+ entry causes calcium induced calcium release through CICR Channels in the sarcoplasmic reticulum. 25% of calcium comes through the sarcolemma from L-type calcium and 75% from the SR.


How is the calcium returned back into the cellular stores/outside the cell?

Most goes back into the SR by the SERCA protein and some leaves the cell althogether through the sodium calcium exchanger and the calcium ATPase.


What chemcial reaction must occur for vascular smooth muscle contraction to take place?

For the smooth muscle to contract the regulatory lite chain on the myosin head must be phosphorylated.


How are myosin light chain heads phosphorylated after depolariation?

For this to happen depolarisation opens VGCCs which releases Ca2+ into the cell. 4 of these Ca2+ bind to CaM (Calmodulin) which in itself binds to Myosin light chain kinase (MLCK) and this enzyme can then phosphorylate the myosin head.


How is the myosin light chain head phosphorylated by neural stimulation of nor adrenaline?

The calcium can also come from the SR which is stimulated to be released by the activation of alpha 1 adreno receptors (activated by noradrenaline). This is a G coupled protein which produces IP3 (inosotol triphosphate) which stimulates the release of Ca2+ form the SR.


What is MLCP and what is it’s purpose?

Myosin light chain phosphatase (MLCP) regulates smooth muscle contraction by de-phopshorylating the myosin light chain head. MLCP is always active (constiuitvely active).


How is MLCP regulated?

When the G protein produces IP3 it also produces DAG (di acyl glycerol) which activates protein kinase C (PKC), this phosphorylates the MLCP inhibiting it.