ACTION POTENTIAL CHARACTERISTICS OF SPECIALIZED CELLS
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Transcript of ACTION POTENTIAL CHARACTERISTICS OF SPECIALIZED CELLS
ACTION POTENTIAL CHARACTERISTICS OF SPECIALIZED CELLS d The
action potential curve shown here is demonstrated by which of the
following?
SA node Atrial muscle Purkinje fibers Ventricular muscle Learning
Objectives Action potential in SA and AV nodes and the effects of
sympathetic and parasympathetic nervous system on them Conduction
pathways in heart and the velocity of conduction Automaticity of
various heart cells the slow response, occurs in the sinoatrial
(SA) node, which is the natural pacemaker region of the heart, and
in the atrioventricular (AV) node, which is the specialized tissue
that conducts the cardiac impulse from the atria to the ventricles
Slow response- SA and AV nodes
The resting potential of slow fibers is less negative Lack the
early repolarization phase (phase 1). The slope of the upstroke
(phase 0), the amplitude of the action potential, and the overshoot
are lesser. RRP in the slow fibers extends well into phase 4 after
the fibers have fully repolarized. The action potential amplitude
and the steepness of the upstroke are important determinants of
propagation velocity along the myocardial fibers. In slow-response
cardiac tissue, the action potential is propagated more slowly and
conduction is more likely to be blocked than in fast-response
cardiac tissue. Slow conduction and a tendency toward conduction
block increase the likelihood of some rhythm disturbances Slow
response- SA and AV nodes
Slow fibers lack functioning fast channels. depolarization is
slower and the action potential travels more slowly across the
surface of the cell. Unstable membrane potential during phase 4;,
(there is a slow, gradual depolarization toward threshold.) Once
the threshold is reached, an action potential is generated.
Characteristics of SA Nodal Cells
depolarization is achieved mainly by influx of Ca++ through L-type
Ca++ channels instead of influx of Na+ through fast Na+ channels.
Repolarization is accomplished in these fibers by inactivation of
the Ca++ channels and by the increased K+ conductance through the
iK1 and iK channels SA Nodal (Pacemaker) Action Potential The if
funny current The funny current is an inward, depolarizing current
through a sodium channel that is unlike every other sodium channel.
This channel is voltage-dependent, but it opens when the cell
repolarizes and closes when the cell depolarizes. As phase 3 ends,
the funny channel opens and causes sodium influx that reverses the
membrane potential and causes the cell to depolarize toward
threshold. Phase 0 Phase 0 is mainly a slow channel (L-type) or
calcium spike rather than a fast channel or sodium spike. Phase 3
As is the case with other action potentials, phase 3 is due to a
rapid potassium efflux (gK increases via iK channels). Pacemakers
Pacemaker ability is conferred on cells by HCN(funny channel). When
open, HCN channels cause Vm to slide gradually toward the threshold
for AP for-mation. The cyclic adenosine monophosphate (cAMP)
dependence of this channel also provides the ANS with a way of
regulating the rate of phase 4 depolarization, which, in turn,
regulates HR. HCN = hyperpolarization activated, cyclic
nucleotidedependent Na channel. SA node is the hearts primary
pace-maker
SA node is the hearts primary pace-maker. It has an intrinsic rate
of 100 beats/min, but HR is usu-ally lower because the PSNS reduces
HR when the prevailing need for cardiac output (CO) is low (see
Figure 17.8B). Should the SA node be damaged and fall silent, then
the AV node takes over as pacemaker. The AV node is normally
subservient to the SA node because its intrinsic rate is 40
beats/min. It takes 1.5 s for AV nodal phase 4 to reach Vth (see
Figure 17.8C), but the new wave of excitation originating in the SA
node typically ar-rives well before this time (overdrive
suppression). Purkinje cells are tertiary pacemakers. Their
intrinsic rate is very low (20 beats/min), partly because Vm is
about 25 mV more negative in Purkinje cells than nodal cells, and,
thus, it takes much longer for Vm to reach and cross threshold from
this more negative level (see Figure 17.8D) Characteristics of AV
nodal cells
The AV nodal action potential is similar to the SA nodal action
potential but differs in that the AV node has a slower rate of
phase 4 depolarization. Because the SA node reaches threshold
sooner, it is the pacemaker of the heart. AV nodal conduction
velocity depends on the rate of rise and the height of phase 0
(inward Ca2+current). REGULATION Regulation: Because HR is a
primary determinant of CO, the SA node is heavily regulated by the
ANS. The SNS increases HR by releasing norepinephrine onto beta
1-adrenergic receptors on nodal cells. These are G proteincoupled
receptors (GP-CRs) that increase adenylyl cyclase (AC) activity and
intracel-lular cAMPconcentration. cAMP binds to and increases HCN
open probability and accelerates the rate of phase 4
depolariza-tion ( Figure 17.9). HR thus increases (positive
chronotropy). PSNS terminalsrelease acetylcholine (ACh) onto nodal
cells. ACh binds to muscarinic type-2 receptors, which are also
GP-CRs that depress AC activity and decrease cAMP formation. The
rate of phase 4 depolarization slows, and HR decreases (nega-tive
chronotropy). Effect of sympathetics
The slope of the pacemaker potential increases, threshold is
reached sooner, and the intrinsic firing rate increases. Activation
of -adrenergic receptors causes increased funny current (sodium)
andincreased calcium current ( gCa). Effect of sympathetics
Sympathetics increase the conductance to Ca2+ and increase the rate
of rise and height of phase 0. This increases the conduction
velocity (decreases the PR interval). normal Sympathetic Effects on
SA Nodal Cells Effect of Parasympathetic stimulation: RMP becomes
more negative, decreased phase 4 slope(opening of Ach sensitive K
channels) Effect of parasympathetics
Parasympathetics hyperpolarize the cell via increasing potassium
conductance. Thus, it takes longer to reach threshold, and the
intrinsic firing rate decreases. There is also a decrease in the
slope of the pacemaker potential caused by reduction of the sodium
funny current and decreased gCa. Effect of parasympathetics
Parasympathetics increase K+ conductance. The persistent increase
in the outward K+ current counteracts the inward Ca2+ current and
decreases the rate of rise and the height of phase 0. This slows
the conduction velocity (increases the PR interval). Adenosine
increases K+ conductance, slows conduction velocity through the AV
node, and is used to stop supraventricular tachycardias (SVT).
Parasympathetic Effects on SA Nodal Cells Regulation of Heart
rate
Sympathetic & parasympathetic (vagus) nerves control the heart
beat rate. A normal heart beat is maintained by slow continuous
discharge from sympathetic nerves The vagal fibers are distributed
mainly to atria than ventricles Without neuronal influences, SA
node will drive heart at rate of its spontaneous activity Normally
Symp & Parasymp activity influence HR (chronotropic effect)
Mechanisms that affect HR: chronotropic effect Positive increases;
negative decreases Autonomic innervation of SA node is main
controller of HR Symp & Parasymp nerve fibers modify rate of
spontaneous depolarization Regulation of Heart rate
Strong sympathetic stimulation can increase the heart rate from
normal 70 beats / min. upto beats / min. Strong vagal stimulation
bring down the rate to beats/min & also can decrease strength
of heart muscle contraction by 20-30% . 14-8 of changes in pressure
in isolated carotid sinuses on neural activity in cardiac vagal and
sympathetic efferent nerve fibers OTHER MECHANISM Local
strech,(resp) Temp K Ca Thyroxine Limbic sys
reflexes Conduction system of the heart: SA node is the pacemaker??
conduction of cardiac impulse Conduction Pathways and Velocity of
Conduction
SA node atrial muscle AV node (delay) Purkinje fibers ventricular
muscle Velocity Fastest conducting fiber = Purkinje cell Slowest
conducting fiber = AV node Automaticity SA nodal cells: Highest
intrinsic rate, primary pacemaker of the heart (100120/min) AV
nodal cell: Second highest intrinsic rate, secondary pacemaker of
the heart (4060/min) Purkinje cells: Slower intrinsic rate
(3040/min) If Purkinje cells fail to establish a rhythm, then
ventricular cells may spontaneously depolarize and produce a
ventricular beat. However, the frequency is very low and
unreliable. Which of the following has the fastest conducting
fibers in the heart?
SA node Atrial muscle AV node Purkinje fibers Ventricular muscle
Which of the following conditions at the A-V node will cause a
decrease in heart rate?
A) Increased sodium permeability B) Decreased acetylcholine levels
C) Increased norepinephrine levels D) Increased potassium
permeability E) Increased calcium permeability Which of the
following best explains how sympathetic stimulation affects the
heart?
A) Permeability of the S-A node to sodium decreases B) Permeability
of the A-V node to sodium decreases C) Permeability of the S-A node
to potassium increases D) There is an increased rate of upward
drift of the resting membrane potential of the S-A node E)
Permeability of the cardiac muscle to calcium decreases ORIGIN
& SPREAD OF CARDIAC IMPULSE