BIOL 253

• In cell signaling, permeability, transport protein availability/expression, lipid or water solubility all directly alter a cell protein's ability to bind to a receptor
• First messengers are signaling molecules (hormones/neurotransmitters) that have to reach the cell and bind to a receptor
• In lipid-soluble, there's no receptor in the cell surface but it's in the nucleus
• In water-soluble, the receptors are located outside the cell
• In water-soluble cells, receptors have a ligand-gated ion channel causing a change in membrane potential and/or cytosolic Ca2+
• In GPCR, the first messenger causes receptor shape change so that the alpha subunit now binds from GDP to GTP (hydrolysis). This then binds to an effector protein (ion channel or enzyme) and generates either a change in membrane potential or second messengers
• After GTP hydrolysis, the alpha subunit is now bound to GDP and return to G protein complex (reunites with beta and y)
• Some GPCRs associate with multiple receptor proteins and some receptors associate with multiple GPCRs
• cAMP is a second messenger that activates a cAMP-dependent protein kinase and causes the phosphorylation of proteins (amplification cascade)
• An example of cAMP is the breakdown of triglyceride in adipose cells and stimulation of glycogenolysis and gluconeogenesis in the liver
• In systole, the AV valves are closed in both isovolumetric ventricular contraction and ventricular ejection. The aortic and pulmonary valves are closed in contraction but open in ejection
• In diastole, the AV valves are closed in isovolumetric ventricular relaxation and open in ventricular filling (atrial contraction). The aortic and pulmonary valves are closed in both relaxation and filling
• In systole, ventricular pressure is greater than aortic pressure
• During ejection in systole, the blood flows out of the ventricle through the aorta or pulmonary trunks
• Before atrial contraction in diastole, 80% of filling occurs is most of it is completed during early diastole
• In systole, once the ventricles contract, pressure increases rapidly causing the volume of the ventricles to decrease as ejection happens
• In diastole, ventricular pressure decreases while ventricular volume increases corresponding to the rapid filling phase
• In the cardiac cycle, blood travels down its pressure gradient: high to low
• A heart murmur is turbulent blood flow through the heart and can be detected using a stethoscope
• Blood flowing in faster and weird directions in a narrowed valve (stenosis) and blood flowing backwards in a leaky valve (insufficiency - a septal birth defect) can lead to a heart murmur
• Cardiac Output = Stroke Volume x Heart Rate
• Stroke Volume = End Systolic Volume - End Diastolic Volume
• The heart is controlled by chronotropic, dromotropic, and ionotropic properties
• Chronotropic is the timing of the node firing; the heart rate itself --> Sympathetic and Parasympathetic stimulation
• Parasympathetic stimulation slows the intrinsic heart rate as acetylcholine binds to cholinergic receptors
• Sympathetic stimulation increases the intrinsic heart rate as epinephrine binds to adrenergic receptors
• Label the Following:

  A) Parasympathetic

  B) Sympathetic

  
• Label the following: As EDV increases, Stroke volume and venous return increases

  A) venous return

  B) end-diastolic volume

  C) stroke volume

  D) stroke volume

  
• Label the following

  A) sympathetic stimulation

  B) increased contractility

  
• What's happening in this image?

  GPCR is activated --> causes the cAMP kinase to activate the L-type Ca2+ channel --> a calcium-induced calcium release occurs through the activation of the ryanodine receptors --> Calcium from this activation causes thin filament activation as calcium binds to troponin --> Crossbridge cycling happens as thick and thin filaments are sliding causing a force generation --> increased force and velocity of contraction

  
• Why is an action potential slower during parasympathetic stimulation?

  F-type channels open slower than normal causing it to make hyperpolarization longer and membrane potential to get to the threshold slower
• F-type channels are activated by voltage and cAMP levels
• During sympathetic stimulation, F-type channels activate more quickly in an action potential causing membrane potential to get to threshold faster
• As plasma epinephrine increases, the activity of sympathetic nerves increases to the heart which increases the heart rate at the SA node. The activity of parasympathetic nerves to the heart decreases
• Sympathetic stimulation, as a dromotropic property, increases conduction velocity through the entire cardiac conduction system
• Parasympathetic stimulation, as a dromotropic property decreases the rate of spread of excitation through the atria and AV node
• What are the three parts of stroke volume?

  Preload, Contractility, and Afterload
• Inotropy is the property where extrinsic factors (typically sympathetic) increase the force of contraction at a given EDV.
• Preload is what's in the ventricles before systole begins; the volume in ventricles just before ejection: end-diastolic volume (EDV)
• As cardiac output increases, venous return increases to maintain equality between the left and right atrium