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Cardiac A&P Flashcards

1
Q

How is cardiac muscle like skeletal muscle?

A
  • Actin and myosin filaments
  • Capable of contracting
  • T-Tubule system and the sarcoplasmic reticulum work to maintain Ca2+ homeostasis
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2
Q

How is cardiac muscle like neural tissue?

A
  • Generates a RMP
  • Can initiate an AP
  • Can propagate an AP
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3
Q

How is cardiac muscle unlike skeletal muscle?

A
  • Tight junctions serve as low resistance pathways to spread AP
  • Cardiomyocytes contain more mitochondria than skeletal muscle cells
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4
Q

Automaticity

A

Ability to spontaneously generate an AP

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5
Q

Conductance

A

Because of their charge, ions do not freely pass through cell membranes; they require an OPEN channel.

An open channel increases conductance; a closed channel reduces conductance.

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6
Q

RMP

A

The difference in electrical potential btwn the inside and outside of cell.
The inside is more (-) compared to outside.

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7
Q

RMP is established by

A
  1. Chemicals
  2. Electrostatic
  3. Na+/K+ ATP-ase
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8
Q

Threshold

A
  • The internal voltage at which the cell depolarizes.

- ALL or NONE

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9
Q

When RMP is closer to threshold potential . . .

A

it is easier to depolarize the cell

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10
Q

When RMP is further from threshold potential . . .

A

it is harder to depolarize the cell

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11
Q

Depolarization

A
  • Takes place when there is a reduced polarity across the membrane
  • There is less charge difference btwn the inside and outside of the cell
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12
Q

Hyperpolarization

A
  • Takes place when increased polarity across membrane

- There is a large difference between the inside and outside

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13
Q

Repolarization

A

Restoration of membrane potential towards RMP

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14
Q

Equilibrium potential

A

Equilibrium is achieved when there is no concentration gradient and there no net flow of ions
*NERNST equation can be used to predict an ion’s equilibrium potential

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15
Q

Nernst equation

A

E ion = -61.5log ([ion] inside/[ion] outside)

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16
Q

K+
-Myocyte
ECF
Equilibrium Potential mV

A

135 mM - myocyte
4 mM - ECF
-94 equilibrium potential

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17
Q

Na+

  • Myocyte
  • ECF
  • Equilibrium Potential mV
A

Na+
10 mM -Myocyte
145 mM - ECF
+60 - Equilibrium Potential

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18
Q

Cl-

  • Myocyte
  • ECF
  • Equilibrium Potential mV
A

Cl-
4 mM - Myocyte
114 mM - ECF
-97 mV - Equilibrium Potential mV

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19
Q

Ca2+

  • Myocyte
  • ECF
  • Equilibrium Potential mV
A

Ca2+
10 mM - Myocyte
2 mM - ECF
+132 - Equilibrium Potential mV

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20
Q

Na/K+ - ATPase

A
  • Removes Na+ gained during repolarization
  • Replaces K+ lost during repolarization
    (3 Na+ out/ 2 K+ in)
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21
Q

Ventricular AP

Phase 0

A

Na+ In

Threshold potential -70 mV; cell depolarizes
Activation of fast v-gated Na+ channels
Slope (steep) indicates conduction velocity (very fast)

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22
Q

Ventricular AP

Phase 1

A

K+ Out
Cl- In

Inactivation of Na+ channels
Cell becomes slightly less (+)
- K+ channels open
- Cl- channels open

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23
Q

Ventricular AP

Phase 2

A

Ca+ In
K+ Out

Activation of slow v-gated Ca+ channels counters loss of K+ to maintain depolarization; it delays repolarization

  • prolongs refractory period
  • sustained contraction necessary for heart pumping
  • Absolute refractory period
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24
Q

Ventricular AP

Phase 3

A

K+ Out
Ca+ In

K+ channels open
K+ leaves faster than Ca+ enters - repolarization
Slow Ca+ channels deactivate
Restarts RMP = -90 mV
*Relative refractory
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25
Q

Ventricular AP

Phase 4

A

K+ out
Na+/K= ATP-ase

K+ leak channels open
- Maintains RMP - 90mV

Na+/K+ ATPase

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26
Q

SA node conduction pathway

A 
SA node
Internodal tracts
AV node
Bundle of HIS
LBB/RBB
Purkinje fibers
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27
Q

The HR is a function of . . .

A
  1. Intrinsic firing rate of dominant PM (usually the SA node)
  2. Autonomic tone
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28
Q

Intrinsic firing rate of SA node

A

70-80 bpm

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29
Q

Intrinsic firing rate of AV node

A

40-60 bpm

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30
Q

Intrinsic firing rate of Purkinje fibers

A

15-40 bpm

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31
Q

How does the SA node set the HR?

A
  • The rate of spontaneous phase 4 depolarization of SA node determines intrinsic HR
  • All cells in the myocardium are capable of automaticity (but with differing rates of depolarization)
  • Cells with fastest depolarization determine how often the heart depolarizes
  • Each times the SA node fires, it depolarizes the reast of the conduction system
  • After the cardiac cycle is complete, the SA is the first to fire again
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32
Q

Autonomic influence on HR

PNS tone

A

CN X - right vagus innervates the SA node and the left vagus innervates the AV node

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33
Q

Autonomic influence on HR

SNS tone

A

Cardiac accelerator fibers T1-T4

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34
Q

SA Node AP

Phase 4

A

Na+ In (f) - funny
Ca+ In (t-type)

Spontaneous depolarization

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35
Q

Describe what is happening in Phase 4 - SA node AP

A

The membrane is leaky to Na
Na+ enters the cell progressively, making it more (+)
Called “funny current” because activated by hyperpolarization, depolarization
At -50mV, transient Ca- channels open to further depolarize all

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36
Q

SA Node AP

Phase 0

A

Depolarization

Ca+ In (L-type)

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37
Q

Describe what is happening in Phase 0 - SA node AP

A

Ca+ enters via v-gated CA+ channels (L-type) - depolarization

Na+ and T-type Ca+ channels close

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38
Q

SA Node AP

Phase 3

A

Repolarization

K+ out

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39
Q

Describe what is happening in Phase - SA node AP

A

K+ channels open
K+ exits the cell, making interior more (-)
K+ efflux - repolarization and the return to Phase 4\
Repolarization decreases Ca+ conductance by closing L-type Ca+ channels

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40
Q

DO2

A

How much O2 is carried in the blood and how fast it’s being delivered to the tissues

Approximately 1000 mL/min

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41
Q

DO2 equation

A

DO2 = CO [(HgbxSaO2x1.34) + (PaO2x0.003)} x 10

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42
Q

CaO2

A

How much O2 is carried arterial blood

Approximately 20 mL/dL

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43
Q

EO2

A

How much O2 is extracted by tissues

25%

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44
Q

VO2

A

How much oxygen is consumed by the tissues

250 mL/min (at rest)

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45
Q

CvO2

A

How much O2 is carried in venous blood

15 mL/dL

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46
Q

Ohm’s Law

A

Current = Voltage difference/Resistance
OR
FLow - Pressure Gradient/Resistance

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47
Q

Flow - Term and Symbol

A

Cardiac output

Q

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48
Q

Pressure Gradient - Term and Symbol

A

MAP-CVP

P1-P2

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49
Q

Resistance - Term and Symbol

A

SVR

R

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50
Q

Poiseuille’s Law

A

Adaptation of Ohm’s Law that incorporates vessel diameter, viscosity, tube length

Q = pie R^4 (P1-P2)/ 8nL

Q = blood flow
R = radius
P1-P2 = arteriovenous pressure gradient
n= viscosity
L = length of tube
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51
Q

Flow

A

Describes the movement of liquid, electricity, or air per unit/time

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52
Q

Flow is directly proportional to

A

the tube radius raised to the 4th power

-Vascular resistance is primarily determined by the r of arterioles - small changes in vessel diameter can have profound effects on flow

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53
Q

Doubling the radius increases the flow by . . .

A

16 x

tripling (r) increase flow 81 x

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54
Q

Laminar flow

A

molecules travel in a parallel path through tube

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55
Q

Turbulent flow

A

non-linear path that will create Eddies

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56
Q

Transitional flow

A

Laminar along vessel walls; turbulent flow in the center

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57
Q

Reynold’s number

A

Can be used to predict if flow will be laminar or turbulent

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58
Q

Re < 2000

A

Laminar flow

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59
Q

Re > 4000

A

Turbulent flow - greater amount of energy lost via heat and vibration = murmur

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60
Q

Re 2000-4000

A

Transitional flow

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61
Q

Viscosity is the result of

A

friction of molecules as they pass through a tube

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62
Q

What is blood viscosity determined by?

A

HCT and temp

  • inversely proportionate to temp
  • proportionate to HCT
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63
Q

O2 delivery (picture flow chart)

A

determined by:

  1. tissue blood flow
  2. CaO2
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64
Q

Tissue blood flow (picture flow chart)

A

determined by:

  1. MAP
  2. Local Vascular Resistance
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65
Q

MAP (picture flow chart)

A

determined by:

  1. CO
  2. SVR
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66
Q

CO (picture flow chart)

A

determined by:

  1. SV
  2. HR
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67
Q

SV (picture flow chart)

A

determined by:

  1. End Diastolic Volume (preload)
  2. End Systolic Volume
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68
Q

EDV (picture flow chart)

A

determined by:

  1. Filling pressures
  2. Compliance
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69
Q

ESV (picture flow chart)

A

determined by:

  1. Afterload
  2. Contractility
70
Q

CO
Formula
Normal Value

A

HR x SV

5-6 LPM

71
Q

CI
Formula
Normal Value

A

CO/BSA

2.8-4.2 L/min/m^2

72
Q

SV
Formula
Normal Value

A

EDV-ESV
CO (1000/HR)

50-100 mL/beat

73
Q

SVI
Formula
Normal value

A

SV/BSA

30-65 mL/beat/m^2

74
Q

EF
Formula
Normal value

A

([EDV-ESV]/EDV) x 100
SV/EDV x 100

60-70%

75
Q

MAP
Formula
Normal Value

A

(1/3 x SBP) + (2/3 x DBP)
(CO x SVR) + CVP/80

70-105 mmHg

76
Q

Pulse Pressure
Formula
Normal Value

A

SBP-DBP
SV output/Arterial tree compliance

40 mmHg

77
Q

SVR
Formula
Normal Value

A

((MAP-CVP)x80)/CO

800-1500 dynes/sec/cm^-5

78
Q

SVRI
Formula
Normal Value

A

([MAP-CVP]/CI )x 80

1500-2400 dynes/sec/cm^-5/m^2

79
Q

PVR
Formula
Normal value

A

((MPAP-PAOP)/CO) x 80

150-250 dynes/sec/cm^-5

80
Q

PVRI
Formula
Normal value

A

([MPAP-PAOP] /CI) x 80

250-400 dynes/sec/cm^-5^m^2

81
Q

Sarcomere

A

the functional unit of the contractile tissue in the heart

82
Q

What things affect sarcomere length and why is this important?

A 
Preload - ventricular wall tension at the end of diastole.   Tension causes stretch/tightness
-Blood volume
-Atrial kick
-Venous tone
-Intrapericardial pressure
- Intrathoracic pressure
Body position
- Skeletal muscle pumping action
83
Q

Ventricular Function Curve illustrates what?

A

rltsp btwn ventricular volume and ventricular output - the Frank Starling Mechanism

  • increase in ventricular volume causes increase in CO
  • occurs up to plateau; after, add’l volume over stretches ventricular sarcomeres and then causes decrease in sarcomeres
84
Q

contractility

A

is the ability of sarcomeres to perform work and is independent of preload and afterload. It is affected by chemicals.
Shorten - produce force

85
Q

Things that increase contractility

A
  • SNS stimulation
  • Catecholamines
  • Ca2+
  • Digitalis
  • Phosphodiesterase inhibitors
86
Q

Things that decrease contractility

A
  • Myocardial ischemia
  • Hypoxia
  • Acidosis
  • Hypercapnia
  • Hyperkalemia
  • Hypocalcemia
  • Volatile gas
  • Propofol
  • BB
  • Ca+ channel blockers
87
Q

Ventricular Function Curve - Upper most curve

A

Increased contractility

“Hyperdynamic”

88
Q

Ventricular Function Curve - Middle curve

89
Q

Ventricular Function Curve - Bottom most curve

A

Decreased contractility
“Heart Failure”
Volume overload

90
Q

Ventricular Function Curve - Y axis

A

CO
SV
LVSW
RVSW

91
Q

Ventricular Function Curve - X axis

A
  1. Filling Pressure
    -CVP
    PAP
    PAOP
    LAP
    LVEDP
  2. End-Diastolic Volume:
    - RVEDV
    - LVEDV
92
Q

Ventricular Function Curve - Bottom of Y axis

A

Hypotension

93
Q

Ventricular Function Curve - Right most X axis

A

Pulmonary congestion

94
Q

Excitation-Contraction coupling

Step 1

A

Depolarization of the myocyte opens v-gated L-type Ca+ channels

95
Q

Excitation-Contraction coupling

Step 2

A

Influx of CA+ turns on the RyR2 receptor which releases Ca2+ from the sarcoplasmic reticulum

96
Q

Excitation-Contraction coupling

Step 3

A

Ca+ binds to troponin C = this is the initiation of contraction

97
Q

Excitation-Contraction coupling

Step 4

A

Ca+ unbinds from troponin C = this is the initiation of relaxation

98
Q

Excitation-Contraction coupling

Step 5

A

Most Ca+ is returned to SR via SERCA2 pump. The Ca+ binds to storage protein calsequestrin.

99
Q

Excitation-Contraction coupling

Step 6

A

Some Ca+ is pumped to cell exterior by Na/Ca+ exchanger

100
Q

Effect of Beta stimulation of excitation-contraction coupling

A
  1. Beta 1 stimulation activates adenylate cyclase which convert ATP to cAMP
  2. cAMP increases production of protein kinase A which activates more L-type Ca+ channels and stimulation of ryanodine 2 receptors to release more Ca+ and stimulations SERCA2 pump to increase CA+ uptake faster
  3. Therefore more forceful contraction in shorter time.
101
Q

Afterload

A

(MAP-CVP)/CO x80

800-1500 dynes/sec/cm^5

102
Q

Pulmonary vascular resistance

A

(mPAP-MAOP)/CO x 80

150-250 dynes/sec/cm^-5

103
Q

Law of Laplace - wall stress

A

Wall stress = (Intraventricular pressure x Radius)/ventricular thickness

104
Q

Wall stress is reduced by . . .

A

decrease in ventricular pressure
decrease in radius
increase in wall thickness

105
Q

Draw Wiggers Diagram and match to ECG

A
  • Isovolumetric Contraction
  • Ventricular Ejection
  • Isovolumetric Relaxation
  • Rapid ventricular filling
  • Reduced ventricular filling
  • Atrial systole
  • AV opens
  • AV closes
  • MV opens
  • MV closes
  • Dicrotic notch
  • Aortic pressure waveform
  • LV pressure waveform
  • LV volume
106
Q

Isovolumetric ventricular contraction

  • MV Position
  • AV Position
A

SYSTOLE

  • Closed
  • Closed
107
Q

Isovolumetric ventricular contraction

key events

A

LV pressure>LA pressure = MV closes
LV Pressure increase
LV volume is constant

108
Q

Ventricular Ejection

  • MV Position
  • AV Position
A

SYSTOLE

  • Closed
  • Open
109
Q

Ventricular Ejection

key events

A

LV pressure>Aortic pressure = AV opens
SV is ejected into aorta
Most SV is ejected during first 1/3 of systole

110
Q

Isovolumetric Ventricular Relaxation

  • MV Position
  • AV Position
A

DIASTOLE

  • Closed
  • Closed
111
Q

Isovolumetric Ventricular Relaxation

key events

A

Aortic pressure> LV pressure = AV closes (2nd Heart sound)
LV pressure decreases
LV volume constant

112
Q

Dicrotic notch (incisura)

A

onset of AV closure causes a short period of retrograde flow from aorta towards AV followed by termination of retrograde flow upon complete AV closure

113
Q

Lusitropy

A

Relaxation

Requires ATP to pump Ca+ back into SR

114
Q

Rapid Ventricular Filling

  • MV Position
  • AV Position
A

DIASTOLE

  • Open
  • Closed
115
Q

Rapid Ventricular Filling

key events

A

LA pressure> LV pressure = MV opens
LV pressure constant
LV volume increase
80-% LV filling happens here

116
Q

Reduced Ventricular Filling

  • MV Position
  • AV Position
A

DIASTOLE

  • Open
  • Closed
117
Q

Reduced Ventricular Filling

key events

A

LV filling continues but at a slower rate

118
Q

Atrial systole

  • MV Position
  • AV Position
A

DIASTOLE

  • Open
  • Closed
119
Q

Atrial systole

key events

A

LA contraction = Atrial kick contributes to last 20% of LV filling
End of atrial systole correlates with EDV

120
Q

Ventricular volume loop curve

6 stages

A
  1. Rapid filling - diastole
  2. Reduced filling - diastole
  3. Atrial kick - diastole (end of bottom of loop)
  4. Isovolumetric contraction - systole (left side of loop)
  5. Ejection - Systole (upward curve to right)
  6. Isovolumetric relaxation - Systole - (left side of loop)
121
Q

Height of ventricular volume loop curve measures?

A

ventricular pressure

122
Q

Width of ventricular volume loop curve measures?

A

Ventricular volume

123
Q

Corners of ventricular volume loop curve measures?

A

Where valves open and close

124
Q

Net external work output of ventricular volume loop curve measures?

A

Myocardial work

125
Q

Phase 1 - Ventricular Filling (diastole)

A

LV volume is about 50 mL (end systolic volume)
LV pressure is 2-3 mmHg
MV opens and ventricular filling begins
Aortic valve stays closed
Since LV is compliant, filling doesn’t increase pressure
Atrial kick increases LV pressure 5-7 mmHg
LV fills to about 120 mL (EDV)

126
Q

Phase 2 - Isovolumetric contraction (systole)

A 
LV is stimulated contract
LV pressure exceeds LA pressure
MV closes
Aortic valve is still closed
LV builds tension and increased LV pressure 
LV volume does not change (X axis)
127
Q

Phase 3: Ventricular Ejection (systole)

A 
LV pressure exceeds aortic pressure
AV opens
MV still closed
LV ejects SV = about 70nmL
As SV enters aorta, LV volume decreases
Normal ESV about 50 mL
DBP is measure where aortic valve opens
SBP is measure at peak of ejection curve
128
Q

Phase 4: Isovolumetric Relaxation (Diastole)

A 
Aortic pressure exceeds LV pressure
Aortic valve closes
MV remains closed
LV volume does not change
LV returns to starting pressure 2-3 mmHg
LV returns to starting value = 50 mL
129
Q

Coronary Circulation Pathway

A

Aorta > RCA and LCA

RCA to Posterior descending artery and Marginal artery

LCA to Circumflex artery and Anterior Interventricular

Small cardiac vein, Middle cardiac vein, Great cardiac Vein > Coronary Sinus

130
Q

What coronary arteries supply blood to the entire heart?

A

the right and left CA

  • first branches off the aorta
  • Arise at the sinus of Valsalva at the aortic root
131
Q

What vessel supplies the SA node?

A

SA nodal artery

  • originates in RAC in 50-60%
  • originates from circumflex in 40-50%
132
Q

Coronary artery dominance

A

the coronary vessel that feeds the PDA determines dominance

  • RCA supplies PDA = r dominance = 80%
  • CxA supplies PDA = left dominance
  • RCA and CxA supply PDA = co-dominance
133
Q

Three main coronary veins

A
  1. great cardiac vein (LAD)
  2. Middle cardiac vein (PAD)
  3. Anterior cardiac vein (RCA)
134
Q

Bipolar leads

A

I - Lateral, CxA
II - Inferior, RCA
III - Inferior, RCA

135
Q

Limb leads

A

aVR
aVL - Lateral, CxA
aVF- Inferior, RCA

136
Q

Precordial Leads

A 
V1 - Septum, LAD
V2 - Septum, LAD
V3 - Anterior, LAD
V4 - Anterior, LAD
V5 - Lateral, CxA
V6 - Lateral, CxA
137
Q

Best TEE view for MI

A

midpapillary short axis

138
Q

Coronary blood flow

A

Coronary perfusion pressure/coronary vascular resistance

139
Q

Coronary reserve

A

Difference between coronary blood flow at rest and at maximal dilation. It is the ability of coronary dilation to increase blood flow in times of stress or exercise

140
Q

Coronary perfusion pressure

A

Aortic DBP - LVEDP

141
Q

coronary autoregulation

A

coronary blood flow is autoregulated between a MAP of 60-140 mmHg. This allows a constant coronary blood flow over a wide range of BP. When MAP falls below range of autoregulation, entirely dependent on CPP

142
Q

coronary autoregulation is net effect of . . .

A
  1. local metabolism - adenosine
  2. myogenic response
  3. ANS
143
Q

Causes of coronary artery constriction

A

Alpha (epicardial) - Increase in IP3 causes increases in intracellular Ca+

Histamine 1 - INcrease in IP3 causes increase in intracellular Ca+

144
Q

Causes of coronary artery dilation

A

Beta 2 (endocardial) - increases in cAMP - causes decrease in intracellular Ca+

Histamine 2 - increase in cAMP - causes decrease in intracellular Ca+

Muscarinic - increase in NO

145
Q

Estimate the coronary perfusion pressure:

A

Aortic DBP - LVEDP

146
Q

Left1. coronary perfusion

A

LV sub-endocardium is best perfused during diastole
As aortic pressure increases, the LV tissue compresses its own blood supply and decreases blood flow. This is systole. This increases coronary vascular resistance and predisposes to ischemia.
B/c epicardial vessels lay on top of heart, they are not compressed during systole.

147
Q

Right coronary perfusion

A

The sub-endocardium of RV is well perfused throughout entire cardiac cycle. This is b/c RV has a thinner wall and does not generate pressure high enough to occlude its circulation.

148
Q

Things that decrease O2 delivery

A
  1. Decreased coronary flow
  2. Decreased CaO2
  3. Decreased O2 extraction
149
Q

Examples of decreased coronary flow

A

tachycardia
decreased aortic pressure
decreased vessel diameter (hypocapnia)
increased EDP

150
Q

Examples of decreased CaO2

A

Hypoxemia

Anemia

151
Q

Examples of decreased oxygen extraction

A

Left shift of Hgb dissociation curve (decreased P50)

Decreased capillary density

152
Q

Things that increase O2 demand

A 
Tachycardia
HTN
SNS stimulation
increased wall tension
increased EDV
Increased afterload
increased contractility
153
Q

What factors affect supply AND demand of oxygen?

A

heart rate, aortic diastolic pressure, preload

154
Q

Tachycardia - affect on supply and demand

A
  1. decreased supply
    - decreased diastolic filling time
    - less time to deliver O2 to LV (RV isn’t affected)
  2. increased demand
    - cardiac contraction and relaxation require ATP
    - incrase # of cardiac cycles/min which increases ATP and O2 utilization
155
Q

Aortic Diastolic Pressure - affect on supply and demand

A
  1. increased supply
    - increased aortic pressure increases pressure that perfuses the coronary arteries (P1-P2_
    - increased Aortic DBP-LVEDP = increase in CPP
  2. increased demand
    - at same time, increase in aortic pressure increases wall tension and afterload. Myocardium requires more O2 as it generates higher pressure to open aortic valve
156
Q

Preload - affect on supply and demand

A
  1. Decreased supply
    - an increased EDV causes a decrease in CPP
    - Aortic DBP- increase in LVEDP = decrease in CPP
  2. Increase in demand
    - increased preload causes increased wall stress
157
Q

The importance of CA in vascular smooth muscle

A

Ca+ has key role in the regulation of peripheral vessel diameter
-increase in Ca= vasoconstriction and v/v

158
Q

Three pathways that affect intracellular Ca+ concentrations:

A
  1. G-protein cAMP pathway - vasodilation
  2. Nitric oxide cGMP pathway - vasodilation
  3. Phospholipase C pathway - vasoconstriction
159
Q

cAMP pathway

A

Increase in Protein Kinase A causes decrease in intracellular Ca+ in the vascular muscle cell
PKA manipulates the excitation-coupling pathway by
1. Inhibition v-gated Ca+ channels in sarcolemma
2. Inhibition of Ca+ release from the SR
3. Reduced sensitivity of the myofilaments to Ca+
4. Facilitation of Ca reuptake into SR via the SERCA2 pump

160
Q

Example of cAMP pathway

A

NE>Beta2>Gs g-protein> Adenylate cyclase> cAMP > Protein Kinase A> decrease in Ca+ > vasodilation

161
Q

what produces NO?

A

NO is produce by ACh, substance P, bradykinin, serotonin, thrombin, shear stress

162
Q

NO/cGMP pathway

Step 1

A
  1. NO synthaetase catalyzes conversion of L-arginine to NO
163
Q

NO/cGMP pathway

Step 2

A
  1. NO diffuses from endothelium to smooth muscle
164
Q

NO/cGMP pathway

Step 3

A
  1. NOP activates guanylate cyclase
165
Q

NO/cGMP pathway

Step 4

A
  1. Guanylate cyclase converts guanosine triphosphate to cyclic guanosine monophosphate
166
Q

NO/cGMP pathway

Step 5

A
  1. Incrase in cGMP reduces intracellular Ca+, leading to relaxation of smooth muscle
167
Q

NO/cGMP pathway

Step 6

A
  1. Phosphodiesterase deactivates cGMP to guanosine monophosphate
168
Q

Phospholipase C pathway activators

A

phenylephrine, NE, angiotensin II, endothelin-1

169
Q

Phospholipase C pathway example

A

Angiotensin II > ATII receptor > Gq g protein > Phospholipase C > IP3 and DAG > Incarease in Ca+ > Vasoconstriction

170
Q

Phospholipase C pathway

A

activation of pathway increases production of two second messengers: IP3 and DAG. IP3 augments Ca+ release from SR and DAG activates protein kinase c. This opens v-gated Ca+ channels in the sarcolemma and increases Ca+ influx.

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