Physiological Science 111B Module 2 Lecture 3

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With regard to cardiac function, what does the nervous system determine?: The frequency that the heart beats and the strength of each contraction.
Automaticity & Rhythmicity: Cardiac function does not solely depend on intact nervous system pathways. The heart has an ability to beat on its own, called AUTOMATICITY, and to control the periodicity of pacemaker activity, called RHYTHMICITY.
Cardiac Electrical Pathway: SA Node (Instrinsic Pacemaker; determines contraction frequency) spontaneously depolarizesÂ„Â³AV Node (and then rest of atria)Â„Â³Bundle of HisÂ„Â³L/R bundle branches in interventricular septumÂ„Â³Purkinje fibersÂ„Â³VentriclesÂ„Â³contraction from ventricles to atria in a squeezing, twisting motion. Improper transmission of the electrical signal can result in arrhythmia.
Beats Per Minute (BPM) SA Node Resting Heart Rate (Resting HR) AV Node Purkinje: The SA Node spontaneously depolarizes at ~100BPM. However, in vivo the resting Heart Rate (HR) is around 70BPM due to ANS control. The AV Node spontaneously beats at 45-50BPM. The Purkinje can beat spontaneously at ~30BPM.
Fast Response AP Slow Response AP: Cardiac cells are characterized by 2 distinct AP patterns that differ significantly from the nervous system AP. The FAST RESPONSE AP is characteristic of normal myocardial fibers in the ventricles, and in Purkinje fibers. The SLOW RESPONSE AP is found in cells of the SA node and the AV node.
Fast Response AP of myocytes and Purkinje Fibers: PHASE 0: RAPID DEPOLARIZATION
Fast Na+ Channels OpenÂ„Â³ Rapid Na+ Influx
Fast Response AP of myocytes and Purkinje Fibers: PHASE 1: PARTIAL REPOLARIZATION
Some Na+ channels closeÂ„Â³membraneÂ¡Â¦s permeability to Na+ decreases + activation of rapidly-opening potassium channels (Ito) that transiently open.
Fast Response AP of myocytes and Purkinje Fibers: PHASE 2: PLATEAU
This phase is UNIQUE to cardiac cells; membrane potential remains constant ~200msec.
Influx of Ca2+ that balances the efflux of K+. The Ca2+ enters through L-type slow Ca2+ channels, which are the target of blockade in the treatment of angina pectoris, cardiac arrhythmias and hypertension (EX verapamil, nifedipine and diltiazem). There is also a decrease in K+ permeability.
Fast Response AP of myocytes and Purkinje Fibers: PHASE 3: RAPID REPOLARIZATION
K+ permeability increases. In cardiac cells, this is due to a combination of outward K+ currents carried by both inward rectifier and delayed rectifier K+ channels, which repolarize the membrane.
Fast Response AP of myocytes and Purkinje Fibers: PHASE 4: Diastole
Na+ - Fast Response AP Movement Channel Type Conductance Increased By [Blocked by]: Movement - inward
Channel Type - fast
Conductance Increased By Â– N/A
[Blocked by] Â– [TTX]
Ca2+ - Fast Response AP Movement Channel Type Conductance Increased By Notes, [Blocked by]: Movement - inward
Channel Type Â– L-type
Conductance Increased By Â– E, NE (increased contractility)
Notes, [Blocked by] Â– [Ca2+ channel blockers (verapamil)]
K+ delayed rectifier Â– Fast Response AP Movement Channel Type Conductance Increased By Notes: Movement Â– outward
Channel Type Â– delayed rectifier
Conductance Increased By - NE, Ca2+ (speeds repolarization)
Notes Â– activated by depol; inactivated by repol; initiates repol at the end of the AP plateau
K+ inward rectifier Â– Fast Response AP Movement Channel Type Conductance Increased By Notes: Movement Â– outward
Channel Type Â– inward rectifier
Conductance Increased By Â– N/A
Notes Â– establishes resting potential; shut off by depol, opens at end of AP to aid in repol (rectifies)
Tension, Relaxation, Tetanus: In cardiac muscle, tension increases during the plateau phase of the AP while the membrane is depolarized, and tension is maintained for as long as the membrane remains depolarized. Repolarization triggers relaxation. The cardiac muscle is refractory during the period of force generation and thus it is not possible to repetitively stimulate a cardiac muscle to tetany.
Myocardium AP vs Skeletal Muscle AP: Skeletal: Increased firing frequency->tetanus induced b/c AP lasts 2-3ms.
Cardiac: long AP duration corresponds with heart contraction and thus tetanus cannot be induced since the AP is ~300ms. This mechanism is essential to the heartÂ’s relaxation and contraction, and therefore cardiac fxn. If tetanus were inducible, adequate relaxation would not be achieved and the heart would not fill with blood since there would be no diastole.
Slow Response Cardiac AP: Nodal cells do not have fast Na+ channels, and depolarization occurs in response to the closing of K+ and the opening of slow Ca2+ channels, which depolarize the membrane to threshold. The resting membrane potential of nodal cells is usually closer to threshold and depolarizes during diastole (phase 4).
Ca2+ - Slow Response AP (nodal cell) Movement Effect Comments: Movement Â– inward
Effect Â– Depolarization
Comments Â– carried by T-type (Transient-type) Ca2+ channels (initial depol) and L-type Ca2+ channels.
K+ - Slow Response AP (nodal cell) Movement Effect Comments: Movement Â– outward
Effect Â– Hyperpolarization
Comments Â– slowly activates during peak (phase 2) and inactivates during diastole (phase 4)
Autonomic Regulation of Pacemaker Activity: Parasympathetic Innervation of Nodal Cell: The parasym VAGUS nerve releases ACh that binds to m2AChRs in nodal cell membranes to maintain IK+. This hyperpols the cell, decreasing HR, since slope of prepotential decreases to depolarize the membrane to threshold. Also, M2R activation decreases cAMP, thus slowing the opening of the Ca2+-T channels. The decreased pacemaker activity of the SA node is due to the parasympathetic activity dominance at rest. Modulation of the pacemaker rhythm is responsible for the normal resting HR of ~70bpm on average.
Autonomic Regulation of Pacemaker Activity: Sympathetic Innervation of Nodal Cell: Sympathetic innervation of the heart involves the release of NE and its effects are mediated by an increase in cAMP. NE induces a decrease in IK+, shortening the prepotential duration. In turn, ICa2+ is activated more rapidly, leading to an increased rapidity of depolarization.
Parasympathetic Control of Nodal Cells Effect on HR Mechanism of Activation Mechanism of Inactivation: Effect on HR Â– negative chronotropic effect
Mechanism of Activation Â– activates G1
Mechanism of Inactivation Â– Cholinesterase breaks down ACh
Sympathetic Control of Nodal Cells Effect on HR Mechanism of Activation Mechanism of Inactivation Other: Effect on HR Â– positive chronotropic effect
Mechanism of Activation Â– activates GS
Mechanism of Inactivation Â– reuptake by mono-amine oxidase (MAO) at the nerve terminal and liver/kidney metabolism by COMT (catachol-o-methyl-transferase)
Other - ~80% NE, ~20% E; reversed in adrenal glands
The control of cardiac function by the nervous system is controlled by the cardiovascular centers in the medulla, which has many inputs:: 1) Carotid and Aortic Bodies: chemoreceptors that respond to elevated CO2 and H+, and depressed O2.
2) Baroreceptors respond to changes in vessel wall stretch, i.e. changes in BP. The Â“baroreceptorÂ” reflex will respond to acute changes in BP.
3) Mechanoreceptors respond to joint movement to help increase blood flow during exercise.
4) Volume receptors in the atria are receptive to changes in blood volume.
Cardiovascular Center of the Medulla 2 Main Divisions Inputs Outputs: Nucleus of the Solitary Tract (NTS)
Cardioexcitatory (SNS): cardiac acceleration & vasoconstriction
Cardioinhibitory: cardiac slowing
Inputs: CNS & Afferent Receptors (chemo, baro, mechano, volume)
Outputs: SNS & PSN (Vagus Nerve)
The 3 Effector Cell Types innervated by the Autonomic Nervous System: 1) Smooth muscle
2) Cardiac muscle
3) Exocrine glands
PNS & SNS example functions: PNS: bradycardia
SNS: Â“fight or flightÂ” response: tachycardia, increased contractility, vasoconstriction, decreased blood flow to skin and viscera, increased blood flow to skeletal muscle
PNS vs SNS Tissue Innervation Pathway Activators and Blockers: COMMON:
-pre/post ganglionic fibers are cholinergic
-preganglionic fibers release ACh
-effect smooth muscle, cardiac muscle, exocrine glands
DIFFERENT:
Released at NEJ: PNS Â– ACh; SNS Â– NE
NEJ Receptors: PNS Â– Muscarinic2; SNS Â– a,b Adrenergic
Activators: PNS Â– ACh, Muscarine; SNS Â– NE & E
Blockers : PNS Â– Atropine ; SNS Â– a-phentolamine & b-propanolol
Receptors and Locations: Nicotinic: ganglia in the ANS
Muscarinic: NEJ in PNS (& in the sympathetic division where cholinergic neurons innervate the skeletal muscle vascular bed)
Adrenergic: neuroeffector junctions in the SNS
Types of Adrenergic Receptors: a1 Â– postsynaptic Â– ex. Smooth muscle contraction
a2 Â– presynaptic Â– ex. Negative feedback to inhibit neurotransmitter release
b1 Â– postsynaptic Â– ex. Heart contractility
b2 Â– postsynaptic Â– ex. Smooth muscle relaxation
b3 Â– postsynaptic Â– ex. Fat cell lipolysis
What is the predominant autonomic tone and how is this known?: PARASYMPATHETIC; if a ganglionic blocker is administered to block ANS function, heart rate increases and blood pressure decreases.
Cardiovascular Organ Responses to SNS and PNS Heart Blood Vessels: HEART
SNS: stimulation, increases HR, increases contractile force
PNS: inhibition, decreases HR
BLOOD VESSELS
SNS: vasoconstriction, Epi Â– vasodilation in skeletal muscle at low concentrations
PNS: (not much innervation)

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