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Quarter 4 > Cardiophysiology Exam I > Flashcards

Cardiophysiology Exam I Flashcards

1
Q

How does contractile tone depend on membrane potential?

A

Depolarization and vasoconstriction are at an increased tone

  • normal basal tone around -50 to -60 mV
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2
Q

Properties of Inward Rectifying (Kir)

A
  • expressed in arterioles
  • open at basal membrane potential
  • open state increased by K+
  • blocked by Ba2+
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3
Q

Roles of Inward Rectifying (Kir)

A
  • supplies part of outward current for basal membrane potential
  • mediates vasodilation by interstital K+ in exercising muscle, myocardium, and brain
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4
Q

Properties of ATP-depnedent (KATP)

A
  • opened by low ATP or raised ADP, GDP, adenosine A1 receptors and [H+]
  • inhibited by alpha-2 adrenoceptors
  • blocked (contraction) by glibenclamide
  • activated (dilated) by diazoxide, pinacidil, cromakalim, nicorandil, CGRP, and VIP
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5
Q

Roles of ATP-dependent (KATP)

A
  • links vascular tone to metabolic state in exercise and hypoxia
  • low, basal open state due to basal PKA activity
  • open state raised in cAMP-PKA-mediated vasodilation
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6
Q

Properties of Voltage-Dependent Kv

A
  • Opens slowly on depolarization beyond -30mV
  • blocked by 4-aminopyridine (4-AP)
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7
Q

Roles of Voltage-Dependent (Kv)

A
  • part of outward current for basal potential in resistance vessels
  • action potential repolarization
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8
Q

Properties of Calcium-Activated (KCa)

(or BK)

A
  • open state promoted by Ca2+ and depolarization
  • strongly expressed in large artery of VSM
  • blocked by tetraethyl ammonium (TEA), iberiotoxin, charybdotoxin, and ethanol
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9
Q

Roles of Calcium-Activated (KCa)

A
  • contributes to basal membrane potential and repolarization
  • if abundantly expressed, BK suppress action potentials
  • provides a “brake” on myogenic contraction
  • implicated in action of NO
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10
Q

Properties of Voltage-Sensitive Ca2+ (VSCC)

A
  • mainly L-type
    • large conductance and long opening
  • abundant in resistance vessels
  • blocked by dihydropyridines
    • Ex: nifedipine
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11
Q

Roles of Voltage-Sensitive Ca2+ (VSCC)

A

supplies inward current for action potentials, graded electromechanical coupling and Bayliss myogenic response

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12
Q

Properties of Receptor-Operated channel (ROC)

A
  • poorly selective between Ca2+, Na+, and K+
  • activated by diacylglycerol when alpha receptors and other G-coupled protein receptors are activated
  • insensitive to Nifedipine
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13
Q

Roles of Receptor Operated channel (ROC)

A
  • mediates pharmacomechanical coupling by NAd, angiotensin, vasopressin, 5HT, and histamine
  • related channel contributes depolarizing current icat of slow excitatory junction potential (EJP)
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14
Q

Activation of Store-Operated cation channel (cat-SOC)

A

When IP3 discharges the SR Ca2+ store

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15
Q

Role of Store-Operated Cation Channel (cat-SOC)

A

conducts extracellular Ca2+ into VSM when Ca2+ store released from SR

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16
Q

Properties of Stretch-Activated cation channel (SAC)

A
  • activated by stretch
  • inward Na+ and Ca2+ currents cause depolarization and VSCC activation
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17
Q

Roles of Stretch-Activated cation channel (SAC)

A
  • contractile response of VSM to stretch
    • myogenic response
  • autoregulation of blood flow
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18
Q

Properties of Calcium-Activated Chloride Channel (ClCa)

A

Open state promoted by Ca2+ at >200 uM

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19
Q

Roles of Calcium-Activated chloride channel (ClCa)

A
  • Contributes ‘inward’ current iCl for slow EJP
  • depolarizes membrane (more positive)
  • contributes to vasomotion
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20
Q

VSM Contraction Properties

A
  • Sacromere-like unit
    • longer actin filaments allow for greater shortening
  • no striations
  • myosin activation causes contraction
    • force determined by [Ca2+] and its sensitivity
  • long contraction
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21
Q

Homocellular Gap Junctions

A

connexons between cells

  • ion-permeable and electrically conductive
  • connects vascular myocytes
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22
Q

Heterocellular Gap Junctions

(myoendothelial gap junction)

A

endothelial and smooth muscle junction

  • between innermost myocytes of the tunica media and endothelial cells
  • transmit hyperpolarizing signals
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23
Q

Sarcoplasmic Reticulum in VSM

A
  • 2 Types of Calcium release channels
    • IP3-Ca
    • Ryanodine
  • small Ca2+ store
    • CCB (nifedipine) are good resistance vessel dilators
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24
Q

IP3-Ca2+ Release Channel

A

releases the SR calcium store

  • raises cytosolic Ca2+ ‘globally’ and increases vascular tone
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25
Q

Ryanodine Receptor (RyR)

A

release spontaneous bursts of Calcium “sparks”

  • activates nearby Ca2+-dependent K+ channels which hyperpolarize the cell
  • does not cause contraction
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26
Q

Caveolae

A

invaginations within the cell wall that increase SA by 75%

  • thought to be signal pathways
    • contain lots of B-receptors, G proteins, Calcium channels, etc
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27
Q

Depolarizing the cell induces _____

A

vasoconstriction

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28
Q

Effect of Epinephrine on alpha receptors

A

vasoconstriction

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29
Q

Effect on Epinephrine on Beta-2

A

vasodilation

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30
Q

Effect of Histamine on H1 receptors

A

vasoconstriction

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31
Q

Myosin Light Chain Kinase (MLCK)

A
  • phosphorylates the myosin light chains in the presence of ATP
  • cross bridge formation
  • smooth muscle contraction
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32
Q

“Latch State” of VSM

A

slow crossbridge cycling

  • maintains vascular tension
  • consumes less energy
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33
Q

Ion Movement in VSM

A
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34
Q

[Ca2+] cytosolic range in VSM

A

100-350 nM

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35
Q

Ca2+ Sequestration

A

Ca2+-ATPase pump in the SR that removes calcium out of the cytoplasm

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36
Q

Ca2+ Expulsion

A

Ca2+-ATPase pump in the sarcolemma that removes Calcium from the cytoplasm

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37
Q

anything that causes VSCC, ROC, or other cation channels to open results in _____

A

vasoconstriction

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38
Q

Explain hypoxia and the role of K channels

A

Hypoxia increases the fraction of open K channels, leading to hyperpolarization

  • closes voltage-sensitive Ca channels
  • reduces calcium infux
  • contributes to hypoxic vascular relaxation
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39
Q

What ion is unusually high in VSM?

A

chloride

54 intra – 134 extra

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40
Q

Which Potassium channel senses ischemia and contributes to hypoxic vasodilation?

A

ATP-dependent K+

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41
Q

Which potassium channel senses extracellular potassium and contributes to vasodilation in exercising muscle, myocardium, and brain?

A

Inward-Rectifier K (Kir)

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42
Q

KATP-blocker drug

A

Glibenclamide

  • causes partial depolarization and vasoconstriction
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43
Q

KATP-activating drug

A

Nicorandil

  • causes vasodilation
  • nitrodilator used to treat angina
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44
Q

Which potassium channels contribute to resting potential and prevent vasospasm?

A

Voltage-dependent (Kv) and Ca-dependent (BK)

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45
Q

Which Calcium channel mediates depolarization-dependent contraction?

A

Voltage-Sensitive Ca2+ (VSCC)

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46
Q

Which calcium channel mediates depolarization-dependent contraction and contributes to agonist-induced electrical excitation?

A

Ca2+-conducting TRP

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47
Q

When potassium exits the VSM cell, the membrane potential becomes negative and as a result _____

A

less calcium enters the cell

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48
Q

Anything that opens a VSM potassium channel results _____

A

vasodilation

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49
Q

Agonism of Beta1 receptors result in _____

A

chronotropy, inotropy, lucitropy, and dromotropy.

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50
Q

Alpha-1 receptor agonist results in

A

vasoconstriction

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51
Q

Beta2 receptor agonism results in _____

A

vasodilation

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52
Q

Vasoconstrictor agonists examples

A

angiotensin II, vasopressin, serotonin, thromboxane, and endothelin

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53
Q

Alpha-1

A
  • numerous in systemic blood vessels
  • NE > Epi
  • activation leads to depolarization and vasoconstriction
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54
Q

Alpha-2

A
  • numerous in cutaneous blood vessels
  • Epi > NE
  • Decreases KATP conductance
    • depolarization and vasoconstriction
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55
Q

Beta-1

A
  • found in cardiac pacemakers and myocardium
  • NE > Epi
  • increase in heart rate and contractility
    • chronotropy and inotropy
    • cAMP pathway
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56
Q

Beta-2

A
  • found in arterial vessels of myocardium, skeletal muscle, and liver
  • Epi > NE
  • coupled to G-protein: cAMP
  • vasdilation
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57
Q

SR distribution

A
  • If scanty and close to sarcolemma
    • activates Ca-activated chloride channels
    • depolarizing current contributes to slow-rising excitatory junction potential
  • If extensive
    • global rise in cytosolic calcium
    • contraction
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58
Q

Fast Excitatory Junctional Potential (fast EJP)

A
  • initial rapid depolarization
  • ATP mediated
  • binds to purinergic receptor (P2x)
  • conducts Na or Ca
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59
Q

Slow EJP

A
  • triggered by norepinephrine
  • may or may not cause action potentials
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60
Q
A

e - membrane potential

t - contractile tension

  • slow EJP was blocked by prazosin
    • depolarization-independent contraction
  • Fast EJPs will always have an action potential, slow EJPs depend on intensity
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61
Q

Initial Phase of Contraction

A

rapid increase in cytosolic calicum leading to contraction

  • occurs synchronously in all myocytes
  • rise in tension
  • large arteries
    • calcium comes from SR via IP3
  • small arteries
    • influx through VSCC after icat and iCl(Ca)
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62
Q

Phase 2 of Contraction

A

tonic phase

  • decrease in cytosolic [Ca2+] leading to partial depolarization
  • vasoconstriction maintained through calcium sensitization
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63
Q

Calcium Sensitization

A

mediated by rhoA kinase

  • inhibits MLC phosphatase
    • favors phosphorylation and contraction
  • also influenced by protein kinase C-alpha
    • same mechanism as rhoaA
  • increase/maintain contraction with decreased cytosolic levels of calcium
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64
Q

Vasomotion

A

rhythmic contractions that help reduce the net capillary filtration rate

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65
Q

Four mechanisms of Vasodilation

A
  • hyperpolarization
  • cAMP PKA
  • cGMP PKG
  • desensitization to calcium
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66
Q

Hyperpolarization mediated vasodilation

A

decreases opening of VSCCC leading to fall in free calcium and vasodilation

  • Examples
    • skeletal muscle contraction
    • sensory nerve neuropeptides
    • KATP-activating drugs
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67
Q

Vasodilation via Nitric Oxide

A

increases cGMP which activates protein kinase G

  • phosphorylation of phospholamban
  • decrease calcium sensitivity
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68
Q

Calcium Channel Blockers

A

bind to L-type calcium channels

  • smooth muscle relaxation
  • negative inotropy
  • affects phase 0 of pacemaker current
    • negative dromotropy
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69
Q

Therapeutic uses for CCB

A
  • hypertension
    • decrease SVR
  • angina
    • vasodilator and cardiodepressant
      • decrease afterload and oxygen demand
    • dilate coronary arteries and prevent vascular spasm
  • arrhythmias
    • decrease conduction velocity and prolong repolarization
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70
Q

(3) types of CCB

A

dihydropyridines, phenylalkylamine, and benzothiazepine

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71
Q

Dihydropyridines

A

vascular smooth muscle selective CCB

  • decrease SVR
  • powerful systemic vasodilators
  • “-pine”
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72
Q

Phenylalkylamine

A

CCB selective for myocardium

  • decreases myocardial oxygen demand
  • reverses coronary vasospasm
  • decreases HR
  • Verapamil
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73
Q

Benzothiazepine

A

CCB with intermediate selectivity

  • decrease inotropy
  • vasodilator
  • Diltiazem
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74
Q

vascular ‘tone’

A

tension exerted by vascular smooth muscle

  • Determines
    • local blood flow
    • capillary recruitment and capillary pressure
    • arterial pressure
    • central venous pressure
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75
Q

Basal Tone

A

vascular tone of arterial vessels when the tonic sympathetic vasoconstrictor nerve activity is blocked

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76
Q

Extrinsic mechanisms for vascular control

A

controls the needs of entire organism

  • vasomotor nerves
  • circulating hormones
    • Epi, NE, angiotensin, vasopressin, insulin
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77
Q

Intrinsic regulatory mechanisms

A
  • Bayliss myogenic response
  • endothelial secretions
  • vasoactive metabolites
  • autocoids
  • temperature
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78
Q

Responses mediated through Intrinsic mechanisms

A
  • flow autoregulation
  • hyperaemia
  • inflammatory vasodilation
  • arterial vasospasm
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79
Q

Vascular Control Hierarchy

A
  • 1st Tier (least)
    • myogenic response
      • autoregulation
  • 2nd Tier
    • intrinsic regulatory chemicals
      • vasodilators of metabolic hyperemia
  • 3rd Tier (most)
    • extrinsic regulation
      • vasomotor nerves and hormones
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80
Q

Bayliss Myogenic response

A

the contraction of a blood vessel that occurs when intravascular pressure is elevated and, conversely, the vasodilation that follows a reduction in pressure

  • contributes to basal tone
  • stabilizes local tissue blood flow and capillary filtration pressure
    • autoregulation
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81
Q

In what tissues does the myogenic response occur?

A

well developed in brain, kidney, and myocardium

Not in skin

82
Q

Mechanism of the Myogenic Response

A
  1. intraluminal pressure rises
  2. stretches the VSM myocyte
  3. activates TRP stretch sensitive non-selecitve cation channels and Cl channels
  4. depolarization of myocyte
  5. opens L-type Ca2+ channels
  6. rise in cytosolic calcium
  7. constriction of myocyte

longterm maintainted by calcium sensitization

83
Q

What drugs block the myogenic response?

A

TRP-channel blocker (gadolinium), chloride channel blockers, ENaC blocker (amiloride), and CCB

84
Q

What prevents excess myogenic constriction?

A

when a vessel narrows, the shear stress increases, stimulating the endothelium to produce more nitric oxide and EDHT

85
Q
A
  • when the myocyte is stretched, L-type calcium channels are activated causing contraction
  • wall tension maintains response
86
Q

(3) Paracrine vasodilators produced by the endothelium

A

NO, EDHT, and PGI2

87
Q

Roles of Nitric Oxide in vascular control

A
  • continuous modulation of basal tone
  • reduction of basal tone in pregnancy
  • flow-induced vasodilation
  • vasodilation mediated by cholinergic parasympathetic fibers
  • vasodilation for sexual erection
  • vasodilation during inflammation and shock
88
Q

Nitrix Oxide and Basal vascular tone

A
  • increased flow or viscosity increases the shear stress
    • produces NO causing vasodilation
  • increased insulin and estrogen
    • increase cardiac output, but decrease in MAP
89
Q

Nitric Oxide and Inflammation

A

inflammatory autocoids (bradykinin, thrombin, and substance P) produce vasodilation by activating eNOS

90
Q

Nitrate Drugs

A

mimic endothelial nitric oxide

  • Nitroglycerin
    • venodilator
      • decrease in CVP leads to decreased preload, SW, and VO2
  • Sodium Nitroprusside
    • arterial and venous dilator
  • Isordil
    • venodilator that decreases CVP
91
Q

Endothelin

A

vasoconstrictor produced by endothelium

  • activates calcium channels and increases cytosolic Ca2+
  • vasoconstriction and venoconstriction lasts 2-3 hours
92
Q

Pathological causes of increased endothelin production

A
  • cerebral vascular hemorrhage, stroke, or brain trauma
    • contributes to verebral vasospasm
    • blocked by bosentan
  • heart failure
    • renal and peripheral vasoconstriction
  • hypoxia
    • pulmonary hypertension and formation of pulmonary edema
  • pre-eclampsia
    • systemic hypertension
93
Q

Metabolic hyperaemia

(functional hyperemia, metabolic vasodilation)

A

when the metabolic activity of an organ increases, the blood flow to the active region increases

94
Q

Metabolic vasoactive factors

A
  • acidosis
  • hypoxia
  • adenosine
  • potassium
  • phosphate
  • hyperosmolarity
95
Q

Interstitial K role in metabolic hyperemia

A

released by active tissues due to repeated depolarization

  • increase extracellular [K+]
    • hyperpolarization causes less calcium entry through VSCC
  • vasodilation
96
Q

Acidosis role in metabolic hyperemia

A

vasodilation

  • increased CO2 and lactic acid production cause vasodilation
  • cerebral blood vessels are particularly sensitive to changes in CO2
  • vasodilation via hyperpolarization and endothelial NO rlease
97
Q

Hypoxia role in metabolic hyperemia

A

arteriolar vasodilation (usually)

  • when PaO2 < 40 mmHg
  • KATP and Kir channel activation
  • fall in Ca2+ sensitivity

vasoconstriction can rarely be seen in pulmonary vessels (HPV) and when hypoxic sympathetic fibers release norepinephrine causing vasospasm in large systemic arteries

98
Q

Adenosine role in metabolic hyperemia

A

released by exercising skeletal muscle and during hypoxia

  • binds to A2A receptors
    • vasodilation
  • links myocardial metabolic rate to coronary blood flow
  • vasoconstrictor in the kidneys
    • maintains GFR
99
Q

Phosphate and Hyperosmolarity role in metabolic hyperemia

A

vasodilation

  • breakdown of ATP that causes an increase in [phosphate] and [K+]
100
Q

hydrogen peroxide role in metabolic hyperemia

A

hyperpolarizing vasodilator

  • generated from breakdown of superoxide
  • increase as oxygen consumption increases
101
Q

Autocoid regulation

A

vasoactive chemicals that are produced and act locally on cells

  • associated with pathological processes
  • alter VSM tone
    • Ex: histamine, bradyknin, serotonin, prostaglandins, thromboxane, leukotrienes, PAF
102
Q

Histamine

A

mediator of inflammation that is stored in mast cells and basophilic leukocytes

  • H1 receptor
    • increase vascular permeability on venules
  • H2 receptor
    • dilates arterioles
103
Q

Bradykinin

A

produced during inflammaiton from kininogen

  • dilates resistance vessels
    • activation causes NO or EDHF production
  • increases venular permeability
  • produces pain
104
Q

Serotonin (5HT)

A

made from AA tryptophan causing vasoconstriction, venular permeability, and pain

  • wide range of effects
  • produced in intestines, endothelium, CNS, and platelets
105
Q

Prostaglandins and Thromboxane

(eicosanoids and prostanoids)

A

derivatives of AA that cause vasoconstriction

  • not inflammatory agents
  • steroids inhibit production of COX
    • NSAIDS are COX 1 and 2 inhibitors
106
Q

Leukotrienes

A

mediators of the inflammatory response that increase vascular permeability

Ex: bronchial inflammation of asthma

107
Q

Platelet activating factor

A

produced during inflammation

  • promotes platelet aggregation
  • bronchoconstriction
  • vasospasm in coronary arteries
  • venular hyperpermeability
108
Q

Metabolic Hyperemia

A

increase in blood flow in proportion to metabolic rate

  • initial cause
    • muscle compression decreases pressure and myogenic response
      • vasodilation and increased flow
  • 2nd phase
    • production and release of metabolic vasodilators
      • K+, adenosine, acidosis, ATP
  • under intrinsic control only
    • myogenic response
  • hyperemia persists after exercise to rebuild oxygen stores
109
Q

Where is autoregulation of blood flow not present?

A

pulmonary circulation

110
Q
A

shifted to the right in hypertensive patients

(kids are shifted to the left)

  • raising or lowering blood pressure transiently raises or lowers blood flow as dicated by Poiseuille’s law
  • myogenic response actively changees the resistance vessel radius, restoring flow close to former level
111
Q

mechanisms of autoregulation

A

primarily by myogenic response

  • then vasodilator washout
    • increased pressure causes increased flow which “washes out” local vasodilator substances
112
Q

Ascending vasodilation during exercise

A

smaller “feed” arteries

  • hyperpolarization of endothelial cells at tissues is conducted through homocellular gap junctions up arterial tree
  • hyperpolarization is then conducted via heterocellular gap junctions to VSM cells
113
Q

Post-Ischemic Hyperemia

A

increase in blood flow followig brief episode of ischemia

  • myogenic response causes vasodilation due to decreased pressure
  • accumulation of vasodilator metabolites from ischemia
    • prostaglandins, hypoxia, lactic acid, etc
114
Q

ischemia-reperfusion injury

A

cellular damage following prolonged periods of ischemia due to slow return of blood flow

(most marked in intestine, liver, and heart)

  • white cell adhesion and activation
  • free oxygen radicals
  • cytosolic calcium overload
115
Q

Sympathetic nervous systemic activation in VSM

A
  1. depolarization reaches terminal axon
  2. fraction of NE released
  3. diffuses across junction
  4. binds to alpha receptor
  5. SM contraction/vasoconstriction
  6. 8-% reuptake and degradation
  7. some NE “spillover” into ciruclation
116
Q

Preganglionic cholinergic fibers

A

activvate nicotinic receptors in sympathetic ganglia

  • travel through the ventral roots of the spinal nerves and white rami communicates
  • enters the sympathetic chains
117
Q

postganglionic nonadrenergic fibers

A

innervate blood vessels

  • send non-myelinated axons through the grey rami communicates into the ventral roots
  • distribution in mixed periphral nerves
118
Q

Neuromodulation

A

neurotransmitter release influenced by chemical environment at varicostiy

  • vasodilator agents inhibit release of NE
    • H+, K+, adenosine, serotonin, ACh
  • vasoconstrictors enchance release
    • angiotensin II
  • negative feedback from NE on alpha-2 pre-junctional receptors
119
Q

Pharmacology of alpha receptor

A
  • vascular myocytes - vasoconstriction
  • NE > Epi
  • antagonists
    • phentolamine and phnoxybenzamine
    • ergotamine
  • therapeutic uses
    • raynaud’s vasospasm
    • acute hypertension
    • migraine
120
Q

Pharmacology of Alpha-1 receptor

A
  • post-junctional receptor on most vessels
    • vasoconstriction
  • NE > Epi and phenylephrine
  • Antagonists
    • prazosin, doxazosin, and terazosin
  • Treatment
    • essential hypertension
121
Q

Pharmacology of Alpha-2 receptor

A
  • autoreceptor of sympathetic varicosity
    • inhibits norepinephrine release
  • receptor in skin vessels and muscle distal arterioles
    • vasoconstriction
  • Epi > NE and clonidine
  • antagonists
    • yohimbine and rauwolscine
122
Q

Pharmacology of Beta receptors

A
  1. SA node and myocardium
    1. increase HR and contractility
  2. arterioles of heart, skeletal muscles, and liver
    1. vasodilation
  3. NE, Epi, and Isoprenaline
  4. Antagonists
    1. propranolol, oxprenolol, and alprenolol
  5. Treatment
    1. angina and hypertension
123
Q

Pharmacology of Beta-1

A
  • SA node and myocardium
    • increase HR and contractility
  • NE > Epi and dobutamine
  • Antagonists
    • atenolol, metroprolol, practolol
  • Treatment
    • angina, hypertension, and arrhythmias
124
Q

Pharmacology of Beta-2 Receptors

A
  • arterioles of heart, skeletal muscle, and liver
  • bronchial smooth muscle
    • dilation
  • Epi > NE, Salbutamol, and terbutaline
125
Q

Phenyleprine

A

alpha-1 agonist

(some alpha-2 and beta-1)

126
Q

Clonidine

A

alpha-2 agonist

(some alpha-1)

127
Q

Dexmedetomidine

A

alpha-2 agonist

(some alpha-1)

128
Q

Epinephrine

(receptor)

A

alpha and beta agonist

(higher Beta-1)

129
Q

Ephedrine

(receptor)

A

alpha-1 and beta-1

(some beta-2)

130
Q

Fenoldopam

(receptor)

A

DA-1

131
Q

Norepinephrine

(receptor)

A

alpha and beta-1

132
Q

Terbutaline

(receptor)

A

Beta-2

(some beta-1)

133
Q

Dobutamine

(receptor)

A

Beta-1

(some beta-2)

134
Q

Dopexamine

(receptor)

A

Beta-2 and DA-2

(some DA-1)

135
Q

Alpha-1 >>>> Alpha-2 antagonist

A

prazosin, terazosin, and doxazosin

136
Q

Alpha-1 > Alpha-2 Antagonist

A

phenoxybenzamine

137
Q

Alpha antagonist example

(alpha-1 = alpha-2)

A

Phentolamine

138
Q

Alpha Antagonist Example

(alpha-2 >> alpha-1)

A

Rauwolscine, yohimbine, and tolazoline

139
Q

Mixed antagonists

Beta-1 = Beta-2 > alpha-1 > alpha-2

A

labetaolol and carvedilol

140
Q

Beta Antagonist Example

(beta-1 >>> beta-2)

A

metoprolol, alprenolol, atenolol, esmolol

141
Q

Beta Antagonist Example

(beta-1 = beta-2)

A

propranolol, timolol

142
Q

Beta Antagonist Example

(beta-2 >>> beta-1)

A

butoxamine

143
Q

(3) main transmitters in sympathetic vasoconstrictors

A

norepinephrine, ATP, and Neuropeptide Y

144
Q

(3) transmitters in parasympathetic dilators

A

ACh, VIP, and NO

145
Q

(3) transmitters in sensory-dilator axons (C-fibers)

A

substance P, CGRP, and ATP

146
Q
A
  • Phentolamine (alpha-blocker) abolishes slow EJP
147
Q

Neuropeptide Y (NPY)

A
  • synthesized in post-ganglionic cell body and transported to sympathetic terminal
  • slower and more prolonged depolarization than ATP
  • sensitizes the post-junctional membrane to norepinephrine (neuromodulation)
148
Q

Sympathetic fibers

A
  • vasoconstrictors that are continuously active
  • reduced sympathetic output causes vasodilation
  • increased output raises peripheral resistance
149
Q

Responses to increased sympathetic activity

A
  • reduced local blood flow
  • decreased organ blood volume
  • capillary pressure decreases due to arteriolar constriction
  • total peripheral resistance increases
150
Q

Mayer waves

A

oscilation of blood pressure due to cyclic changes in sympathetic vasomotor tone driven by a resonance in the baroreceptor reflex

151
Q

Traube-Hering waves

A

oscillations in blood pressure during inspriation and exhalation

152
Q

Parasympathetic System

A
  • long pre - short post
  • limited distribution to VSM
    • not tonically active
  • Cranial PNS nerves (ex: vagus)
    • coronary arteries, salivarly glands, GI
  • Sacral PNS nerves
    • genitalia, bladder, colon
153
Q

Which tissues do not have a parasympathetic innervation?

A

skin and muscle

154
Q

Neurotransmitters of PNS

A
  • primarily acetylcholine
    • hyperpolarization and vasodilation due to NO production on intact endothelium
  • Non-adrenergic, non-cholinergic (NANC)
    • VIP, substance P, and NO
155
Q

Sympathetic Vasodilator nerves

A
  • ACh released
  • vasodilation is transient as there is a limited distribution of cholinergic fibers
  • primarily travels to sweat glands
156
Q

Sympathetic Vasoconstrictor Fiber

A
  • Norepinephrine (and ATP)
  • distributed in most organs and tissue
  • tonically active
  • centrally controlled in brainstem
  • major role in baroreceptor reflex
  • very important role in BP
  • well sustained duration
157
Q

Sympathetic Dilator Nerve

A
  • Acetylcholine (and VIP)
  • distributed only in sweat glands
  • NOT tonically active
  • centrally controlled in forebrain
  • negligible baroreceptor reflex
  • unimportant in BP
  • transient duration
158
Q

Lewis Triple Response

A
  • redness
    • vasodilation along line of scratch
  • local swelling
    • inflammatory edema
  • spreading flare
    • area of redness extending from the site of trauma
    • mediated by sensory nerves
159
Q

Dermatographia

A

extreme triple response where a simple touch leaves welts on the skin

160
Q

Insulin

A

stimulates endothelium to produce NO

  • vasodilator
  • antithrombotic actions
  • inhibits vascular smooth muscle growth and migration
161
Q

Thyroxine

A

induces cardiac myocytes to express high density Beta-1 receptors

  • enhances contractility
  • In hyperthyroidism, there is an increase in basal metabolic rate, leading to vasodilation and a fall in peripheral resistance
    • tachycardia and a rise in stroke volume
162
Q

Estrogen

A

vasodilator by activating NO synthase and BKCa channels

163
Q

Relaxin

A

peptide hormone secreted during pregnancy

  • causes vasodilation in the uterus, mammary glands, and heart
  • attenuates endothelin-mediated vasoconstriction
164
Q

Epinephrine

A
  • Metabolic effects
    • glycogenolysis in skeletal muscle
    • lipolysis in adipose
  • Cardiavascular
    • increased HR and contractility (B-1)
    • arterial and venous constriction (A-1,2)
    • vasodilation in myocardium, skeletal muscle, and liver (B-2)
165
Q

Norepinephrine

A
  • increases BP and peripheral resistance
  • decreases HR and cardiac output

alpha and beta effects, but alpha agonist predominates causing vasoconstriction

166
Q

Vasopressin (ADH)

A

stimulates receptors on collecting ducts leading to increased water reabsorption and the prevention of dehydration

  • stimulated by a fall in blood volume and BP
  • absent in diabetes insipidus
  • produced in hypothalamus and released by posterior pituitary
  • causes vasoconstriction and an increase in plasma volume
167
Q

Angiontensin II

A
  • stimulates aldosterole
    • promotes renal salt and water retention
  • vasoconstriction
    • raises peripheral resistance and BP
  • stimulates the thirst sensation
168
Q

Atrial Natrituretic Peptide

A
  • dilation of resistance vessels
  • increase sal and water excretion
  • fluid transfer from plasma to interstital compartment

counteraccts the effects of the RAAS system

169
Q

Structure of Adrenal Gland

A
  • located on upper pole of kidney
  • outer: cortex
    • steroid hormones (cortisol and aldosterone)
  • inner: medulla
    • catecholamines
170
Q

Triggers for Epinephrine secretion

A

exercise, hypotension, and hypoglycemia

171
Q

Comparison of Epi and NE

A
172
Q

Arterial pressure and HR in Epinephrine

A
173
Q

Arterial pressure and HR in Norepinephrine

A
174
Q

Vasopressin release

A

increased osmolarity and decreased blood pressure stimulates vasopressin release

175
Q

Venous vs Arteriolar Control

A
  • veins have little basal tone in the absence of sympathetic activity
  • do not have myogenic response
  • respond to hormones, autocoids, and drugs differently
176
Q

Stimuli that activate RAAS

A
  • hypotension
  • increased renal sympathetic activity
  • fall in NaCl concentration at the macula densa
  • reduced renal artery pressure
177
Q

Coronary blood flow in resting human

A

70-80 ml/min/100g

(during heavy exercise, 300-400)

178
Q

myocardial oxygen extraction at rest

A

65-75%

179
Q

Oxygen Extraction

A

consumption/delivery

180
Q

When does most coronary artery flow occur?

A

diastole

181
Q

Main risk factors for coronary atheroma

A
  • high LDL
  • hypertension
  • smoking
  • diabetes
  • obesity
182
Q

Coronary artery structure increases likelihood of MI

A

functional end-arteries

(no anastomoses)

183
Q

heart anatomy

A
184
Q

Which coronary recieves a higher blood flow?

A

left

185
Q

The primary method used by the coronary circulation to increase oxygen deliver is _____

A

vasodilation and increased blood flow

186
Q

Unique considerations of Coronary perfusion

A
  • O2 supply is flow limited
    • because extraction fraction is high at rest
  • functional end-arteries
    • prone to atheroma
187
Q

Skeletal Muscle Circulation

A
  • 40% of body mass
    • receives 20% of CO at rest and 80% during exercise
  • high amount of resting vascular tone
    • dense SNS innervation
    • regulation of MAP
188
Q

Tonic (postural) Muscles

A
  • blood flow at rest 15mL/min/100g
  • higher capillary density
    • 15% of all muscle fibers are red (slow)
189
Q

Maximum flow to skeletal muscle can be ______

A

80-90%

190
Q

Acral skin

A

high number of AVAs

  • fingers, toes, lips, nose, ears
  • little basal tone
  • lots of SNS innervation
191
Q

Temperature Regulation

A

warmth receptors in anterior hypothalamus modulate SNS outflow to skin

192
Q

Changes during Hyperthermia

A

core temperature > 37.5oC

  • vasodilation and hyperemia
  • skin on limb and trunk increase sympathetic vasodilation
  • acral skin decreases SNS outflow leading to vasodilation
193
Q

Hypovolemia

A
  • response to low cardiac output is an increase in SNS outflow
    • vasoconstriction and catecholamine secretion to maintain SV
  • forced warming may cause cardiovascular collapse by increasing flow to skin
194
Q

Cerebral Perfusion Pressure equation

A

MAP - ICP

(if ICP > CVP)

MAP - CVP

(if CVP > ICP)

195
Q

Average blood flowin cerebral circulation

A

55 mL/min/100g

196
Q

Autoregulation of cerebral perfusion

A
  • raised arterial CO2 causes vasodilation
  • low CO2 causes vasoconstriction
  • local sympathetic stimulation affects flow significantly only when arterial pressure is high
197
Q

Cushing’s Reflex

A

stimulation of vasomotor center in brainstem due to increased ICP

  • hypertension and reflex bradycardia
198
Q

Cerebral Vasospasm

A

intracerebral hemorrhage

  • release endothelin, serotonin, and neuropeptide Y
199
Q

Migraine

A

due to dilation of large extracerebral vessels

  • Treat with sumatriptan: 5HT-1 agonist
    • vasoconstriction
200
Q

Regulation of Pulmonary Vascular Tone

A
  • perfusion dependent on CO
  • no autoregulation
  • no metabolic hyperemia
  • autonomic NS innervation very small
  • HPV
    • primary influence over vascular tone
201
Q

portal vein

A

70-80% of hepatic blood flow

  • yet contributes equally to O2 supply with hepatic artery
202
Q

Intrinsic regulation of hepatic blood flow

A
  • hepatic artery
    • autoregulation
    • metabolic hyperemia
  • hepatic portal vein
    • no autoregulation
    • in series with splanchnic vessels

Quarter 4 (15 decks)

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