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CVS II > Circulation > Flashcards

Circulation Flashcards

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1
Q

Define vascular tone

A

describes degree of constriction of a blood vessel relative to max dilation

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2
Q

What’s vascular tone controlled by?

A

contractile state of vascular smooth muscle cells (VSMCs)

Tonic sympathetic activity (constriction) + Tonic NO release (dilation)

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3
Q

Which vessels have vascular tone + why?

A

arteries, arterioles, veins

containing VSMCs

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4
Q

Why regulate vascular tone?

A

vital target in treating CVD

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5
Q

How do the substances in blood control vascular tone?

A

Hormones - Adr, Ang II, ADH, ANP
Platelets –TXA2
Immune cells - Histamine
Blood causes stretch

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6
Q

How does the endothelium control vascular tone?

A

PRODUCES:
Dilators = NO, K+, PGI2
Constrictors = ET-1

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7
Q

How do VSMCs control vascular tone?

A

responds to:
substances in blood
substances released from endothelium

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8
Q

How do nerves control vascular tone?

A

Sympathetic vasoconstrictor nerves: NA
Parasympathetic vasodilator nerves: NO, Ach
Sympathetic vasodilator nerves: Ach, VIP
Perivascular sensory nerves nerves: Sub P, CGRP

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9
Q

Where do vasoconstrictor nerves interact at?

A

interact directly at VSMCs

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10
Q

What do vasoconstrictor nerves interact with?

A

indirectly

  • interact with endothelium
  • endothelium interacts with VSMC
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11
Q

How do metabolic factors control vascular tone?

A

Adenosine, K+, H+

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12
Q

Why have intrinsic or local controls?

A

Regulate local blood flow to organs/tissues

Vital in regional hyperaemia

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13
Q

eg of intrinsic or local controls?

A

endothelium, immune cells, platelets, stretch

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14
Q

Why have extrinsic controls?

A

Regulate TPR to control BP for blood flow

Brain alters blood flow to organs during exercise + thermoregulation

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15
Q

What are extrinsic or external controls + eg?

A 
Nerves:
Vasoconstrictors - NA
Vasodilators  - Ach, NO
Hormones:
Vasoconstrictor - A, Ang II, ADH
Vasodilators - ANP
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16
Q

What does stimulated α1 adrenoceptors do?

A

vasoconstriction

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17
Q

What does stimulated β2 do?

A

vasodilation in coronary + skeletal muscle arterioles

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18
Q

Describe how the brainstem control vascular tone?

A
  • sense stress
  • feeds into (RVLM) which receives info from CVLM, hypothalamus
  • Thoraric spinal cord Intermediolateral (IML)
  • short sympathetic preganglionic fibre to sympathetic ganglia/adrenal medulla
  • long sympathetic postganglionic fibre
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19
Q

What’s on post-synaptic membrane?

A

α1 – contraction, α2 – contraction, β2 - relaxation

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20
Q

What’s on pre-synaptic membrane?

A

AT1 – increase release of NA (RAAS ↑ sympathetic)
α2 – ↓ NA release
K+, adenosine – ↓ NA release for vasodilation

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21
Q

Describe what happens at post-synaptic terminal

A
  • AP down postganglionic fibres
  • activate vgccc
  • Ca2+ influx
  • vesicle release of NA
  • NA hit postsynaptic membrane on VSMCs at α1, α2, β2
  • α1 causes vasoconstriction
  • decrease NA by : reuptake, cleared by capillaries, feedback to α2 on pre-synaptic terminal, adenosine + K+
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22
Q

What’s Rostral Ventral Lateral Medulla (RVLM vasomotor centre) controlled by?

A

Caudal Ventro Lateral Medulla (CVLM), hypothalamus

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23
Q

Why’s it vital that sympathetics controlled by brainstem + RVLM?

A

Provides central control of blood flow + BP

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24
Q

Define tonic sympathetic nerve activity

A

sets vascular tone by firing 1 AP/s

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25
Q

What does fall in sympathetic activity cause?

A

vasodilation

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26
Q

Roles of sympathetic vasoconstrictor nerves?

A

-Contract resistance arterioles : produces vascular tone for vasodilatation for increased blood flow
-Distinct RVLM neurones-sympathetic pathways innervate diff tissues : Increased sympathetic nerve stimulation to GI (less blood flow) whilst reduce to skin (more blood flow, cool down)
-Pre-capillary vasoconstriction : ↓capillary pressure due to pressure drop
 absorption of interstitial fluid into blood plasma
to maintain blood volume (important in hypovolemia)

Control TPR - maintains arterial blood pressure and blood flow to brain/myocardium since Pa = CO x TPR and BF = Pa / TPR

Controls venous blood volume (at rest 2/3rd blood in veins)
Venoconstriction   venous blood volume   Venous return
 stroke volume via Starling’s law

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27
Q

Roles of sympathetic vasoconstrictor nerves + eg?

A
  • Contract resistance arterioles : produces vascular tone for vasodilatation for increased blood flow
  • Distinct RVLM neurones-sympathetic pathways innervate diff tissues : Increased sympathetic nerve stimulation to GI (less blood flow) whilst reduce to skin (more blood flow, cool down)
  • Pre-capillary vasoconstriction : ↓capillary pressure due to pressure drop so reabsorption of interstitial fluid into blood plasma maintaining blood volume (vital in hypovolemia)
  • Control TPR : maintains arterial BP + flow to brain/myocardium as Pa = CO x TPR and BF = Pa /TPR
  • Controls venous blood volume : venoconstriction ↓ venous blood volume for venous return by increasing SV via Starling’s law
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28
Q

eg of vasoconstrictors hormones

A

Adrenaline, Angiotensin II, Anti-Diuretic Hormone, Endothelin-1 (EN1), Thromboxane (TXA2)

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29
Q

eg of vasodilator hormones

A

Atrial natriuretic peptide (ANP)

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30
Q

Physiological role of hormonal control of VSMCs?

A

Controls BP + flow during activity

Maintain BP + flow to brain, heart during haemodynamic crisis (haemorrhage, dehydration)

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31
Q

Pathological role of hormonal control of VSMCs?

A

Excess production, associated with excess vasoconstriction + vascular disease – hypertension, heart failure

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32
Q

What’s adrenaline?

A

Released due to sympathetic nerve stimulation
From adrenal glands
Acts on α1-adenoceptors on VSMCs

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33
Q

What’s Angiotensin II (Ang II)?

A

Formed from RAAS
Potent vasoconstrictor
Acts on AT1 receptors on VSMCs

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34
Q

What’s ADH (Vasopressin/Anti-Diuretic Hormone)

A

Released from posterior pituitary

Acts on V1-receptors on VSMCs

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35
Q

What’s Endothelin-1 (ET1)?

A

Released from endothelium

Acts on ET1 receptors on VSMCs

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36
Q

What’s Thromboxane (TXA2)?

A

Released from aggregating platelets
Acts on TP receptors on VSMCs
Vital vasoconstriction alongside clotting process

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37
Q

How is Ang II produced by RAAS system during drop in CO?

A
  • low CO
  • low renal blood flow
  • sympathetic nerves β1
  • low NaCl load
  • produce renin
  • produce angiotensinogen in liver
  • produce Ang I (decapeptide)
  • Angiotensin Converting Enzyme (ACE) on lung vascular endothelium
  • produces Ang II (octapeptide)
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38
Q

How much blood does kidney receive?

A

25% of CO

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39
Q

Why do lungs have ACE?

A

lungs receive total CO

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40
Q

Effects of Ang II?

A
  • ↑sympathetic - central effect
  • ↑Blood volume - adrenal glands release aldosterone NaCl+ H2O Retention
  • ↑TPR - vasoconstriction, stimulates sympathetic nerves
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41
Q

What is ADH produced during a haemorrhage?

A
  • drop in blood volume detected by arterial baroceptors + left atrial receptors
  • switches off Nucleus Tractus Solitarius (NTS)
  • inhibitory pathway switches off CVLM
  • switches on positive pathway of hypothalmic nerves
  • stimulates magnocellular neurons in SON + PVN
  • drives ADH release from posterior pituitary
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42
Q

Effects of ADH?

A
  • ↑blood volume : at kidney V2 receptors, insertion of aquaporin channels in collecting duct so ↑H2O reabsorption
  • vasoconstriction : at VSMCs V1 receptors during hypovolemia
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43
Q

Importance of myogenic response?

A

Maintains local blood flow during changes in local blood pressures
Protective mechanism – BP drops, still good flow – BP high, less flow/damage

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44
Q

What’s the myogenic response?

A

As pressure increases, more distension, more vasoconstriction but blood flow remains the same

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45
Q

How do vasoconstrictors increase vascular tone?

A

by activating same G-protein-coupled pathway in VSMCs

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46
Q

What does receptor does NA work on?

A

α1

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47
Q

What does receptor does Adrenaline work on?

A

α1

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48
Q

What does receptor does Ang II work on?

A

AT1

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49
Q

What does receptor does Vasopressin (ADH) work on?

A

V1

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50
Q

What does receptor does Endothelin-1 (ET-1) work on?

A

ETA

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51
Q

What does receptor does Thromboxane A2 (TXA2) work on?

A

TP

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52
Q

Describe how vasoconstrictors increase vascular tone?

A
  • Stretch activates these receptors – myogenic response
  • receptors are Gq
  • linked to PLC
  • hydrolysis of PIP2 -> DAG + IP3
  • IP3 acts on SR to cause release of Ca2+
  • DAG increases excitability, gets more depolarised, activates vgcc, release of Ca2+
  • influx of Ca2+ from external fluid
  • Ca2+ activates Calmodulin
  • drives myosin light-chain kinase
  • phosphorylation of myosin heads
  • interaction between myosin-actin
  • contraction
53
Q

Effects of Atrial Natriuretic Peptide (ANP)?

A
  • systemic vasodilatation : opposes NA, A, Ang II, ADH, ET-1, TXA2
  • ↓blood volume : dilation of renal afferent arteriole, increase glomerular filtration rate, increased Na+ + H2O excretion by the kidney -
  • ↓release+actions : aldosterone, renin, ADH
54
Q

How vasodilater hormone ANP produced when excess vasoconstriction?

A
  • increase blood volume, too much vasoconstriction
  • more blood returns to heart
  • detected by stretch receptors in atrium
  • release ANP by specialised atria myocytes
  • act at NP receptors on VSMCs - ↑cGMP pathway
55
Q

What’s Atrial Natriuretic Peptide (ANP)

A

Biomarker for poor heart function/congested circulation – e.g. heart failureom atria
-acts on VSMC

56
Q

What receptor does Atrial Natriuretic Peptide (ANP) work on?

57
Q

What are the diff vasodilator responses?

A

Nerves
Endothelium Derived Relaxation Factors (EDRF)
Endothelium Derived Hyperpolarisation Factors (EDHF)

58
Q

What’s sympathetic vasoconstrictor nerves inhibited by?

A

Parasympathetic vasodilator nerves
Sympathetic vasodilator nerves
Sensory (nociceptive C fibres) vasodilator nerves

59
Q

Where are parasympathetic vasodilator nerves + what do they release?

A

Salivary glands – release Ach / VIP

Pancreas + intestinal mucosa – release VIP

60
Q

Why do salivary glands, pancreas, intestinal mucosa need high blood flow?

A
  • need fluids to produce salivia, enzymes, pancreatic juices for excretion
  • maintains parasympathetic-mediated fluid secretion
  • releases juices
61
Q

How does vasodilation happen in salivary glands, pancreas, intestinal mucosa?

A

parasympathetic nerves release Ach/VIP act on endothelium to cause release of NO

62
Q

What does receptor does Ach work on?

63
Q

How does vasodilation happen for erection?

A
  • erectile tissue releases NO by parasympathetic nerves
  • causes production of cGMP
  • vasodilation
64
Q

How does Sildenafil (Viagra) work?

A

enhances NO by blocking breakdown of cGMP by phosophodiesterase 5

65
Q

Where are sympathetic vasodilator nerves + what do they release?

A

Skin (sudomotor fibres) – release Ach, VIP

66
Q

Effect of Ach + VIP on sudomotor fibres?

A

cause release of sweat + vasodilation

67
Q

Importance of sympathetic vasodilator nerves for skin?

A

-need more blood flow, to make more sweat,
-need more blood flow to skin
helps to cool down

68
Q

What’s blushing?

A

Head, face, upper chest blush by stress (sympathetic) response

69
Q

What causes redness in trauma + infection?

A

stimulation of sensory axon reflex (C-fibres)

70
Q

Describe how redness happens in trauma + infection

A

-C fibres (pain fibres) stimulated + releases CGRP
-pain pathway stimulus to dorsal root ganglion in spinal cord + brain perceives pain
-axon collaterals come of C fibres goes to blood vessels + localised immune cells (mast cells):
releases substance P acts at endothelium + VSMC
stimulates mast cells that produce histamine
-vasodilation

71
Q

How does NO cause vasodilation?

A
  • shear stress in endothelium (or IF) stimulates Nitric Oxide Synthase (eNOS)
  • produces NO
  • NO diffuses from endothelium cell into VSMC
  • stimulates G pathway
  • stimulates Guanulate Cyclase (GC)
  • produces cGMP from GMP
  • cGMP activates PKG
  • PKG causes vasodilation
72
Q

Why’s there constant release of NO?

A

Blood flow (via shear stress)

73
Q

What’s Nitric oxide (NO)?

A

lipophilic, soluble gas, freely diffusible

Stimulates GC

74
Q

eg of inflammatory factors?

A

Sub P, histamine, bradykinin, Ach

75
Q

How does Prostacyclin (PGI2) cause vasodilation?

A
  • shear stress (or IF/Ach) on endothelium
  • membrane lipids into PGI2 via cyclooxygenase (COX)
  • PGI2 acts at Prostanoid receptor (PGI2) on VSMC’s
  • drives A pathway
  • Gs -> AC -> cAMP -> PKA
  • PKA causes vasodilation
76
Q

Importance of Prostacyclin (PGI2)?

A
  • tonic PGI2 production
  • vasodilates renal arterioles
  • maintain glomerular filtration rate (GFR) + kidney function
77
Q

Why shouldn’t you give NSAIDs to people with kidney failure?

A
  • COX inhibition
  • reducing PGI2
  • vasoconstriction
  • dangerous in kidney failure
78
Q

Why do PKA + PKG produce vasodilatation?

A
  • ↑Ca ATPase (SERCA) – increase uptake into SR + exclusion from cell
  • ↑K channel activity->hyperpolarisation->VGCCs switched off
  • Inhibits myosin light chain kinase (MLCK)
79
Q

How does endothelium-derived hyperpolarisation factors eg K+ cause vasodilation?

A
  • K+ is 4mmol outside cell
  • shear stress (or IF) activates K+ channels on endothelium
  • release K+ to local external fluid
  • high K+ in local external fluid
  • switches on K+ channels
  • more K+ go out
  • switches on Na/K-ATPase
  • 3Na+ out, 2K+ in
  • hyperpolarisation of VSMC
80
Q

How does endothelium-derived hyperpolarisation (EDH) cause vasodilation?

A
  • shear stress (or IF) activates K+ channels on endothelium
  • conduction of hyperpolarisation from endothelium to VSMCs via gap junctions
  • less VGCCs and Ca entry
81
Q

How does stimulation of β2-adrenoceptors cause vasodilation?

A

increases PKA activity so:

  • ↑Ca ATPase (SERCA) – increase uptake into SR + exclusion from cell
  • ↑K channel activity->hyperpolarisation->VGCCs switched off
  • Inhibits myosin light chain kinase (MLCK)
82
Q

Other functions of endothelium?

A
  • Blood–tissue interactions, production of Ang II, endothelium surface contains ACE
  • Blood clotting, Inflammatory pathway, Angiogenesis, Atheroma
83
Q

How endothelium dysfunction happens?

A

Breakdown of endothelium function by hypertension, diabetes, cigarette smoking
Reduce NO/PGI2 production, enhance vasoconstriction

84
Q

Why’s regulation of BP + BF vital when treating sepsis?

A

BP too low – systolic <60 mmHg

poor drive for end organ perfusion

85
Q

Why’s regulation of BP + BF vital when treating hypertension?

A

BP too high – damage blood vessels, afterload which reduces CO, increasing O2 demand of heart - alters end organ perfusion

86
Q

Darcy’s law equations?

A 
Blood flow (CO) = BP / TPR
BP= CO x TPR
87
Q

Poiseuille’s law equations?

A

TPR ∝ r⁴

88
Q

What controls BP + BF?

A

Regulation of vascular tone (controlling blood vessel radius)

89
Q

Effect of increasing vascular tone?

A

increase blood vessel constriction + BP

90
Q

Effect of reducing vascular tone?

A

induce blood vessel dilation + reduce BP

91
Q

When do you increase vasoconstriction?

A

when a drop in BP in these conditions:

sepsis, anaphylaxis, HF

92
Q

What’s sepsis?

A

-systemic infection –> excessive vasodilatation
-decreases TPR
-drop in BP
-no drive for end organ perfusion
-end organ damage
very serious, ITU (Intensive Treatmeant Unit)

93
Q

What’s anaphylaxis?

A
  • hypersensitivity reaction –> systemic vasodilatation,

- poor end organ perfusion

94
Q

What’s HF?

A
  • poor CO
  • poor BP
  • poor end organ perfusion
95
Q

Which stimulated receptors cause vasoconstriction?

A

α1, AT1, V1, ETA, TP

96
Q

Which pathways are vasoconstrictor receptors?

97
Q

What does Adrenaline act as at GI tract + skin?

A

vasoconstrictor

98
Q

What does NA act as at GI tract + skin?

A

vasoconstrictor

99
Q

What does Adrenaline act as at skeletal muscle + coronary circulation?

A

vasodilator

100
Q

What does NA act as at skeletal muscle + coronary circulation?

A

vasodilator

101
Q

Why are there diff between NA + A?

A

NA has higher affinity for α > β
A has higher affinity for β > α
and skeletal muscle + coronary arteries have more β2 than α1

102
Q

What does A mostly do?

A

dilates vessels at β2

103
Q

What does NA mostly do?

A

constricts vessels at α1

104
Q

What happens if you give Adrenaline via IV?

A 
Acts at β1 heart to:
-increase HR, CO, force of contractility to increase SV
- CO = HR X SV
-increases BP slightly as TPR is reduced
- BP = CO X TPR
Acts at β2 skeletal muscle to:
-dilates vessels reducing TPR
105
Q

What happens if you give NA via IV?

A

Acts at α1 to:

  • increases vasoconstriction + TPR
  • BP increases
  • baroceptors switches off HR, contractility, drop CO
  • protects heart
106
Q

Pharmacological vasoconstrictors agents + eg of when it’s given?

A

NORAD (NA) = sepsis, severe HF
A = epipen for anaphylaxis
ADH (Vasopressin) = sepsis

107
Q

Effects of NORAD?

A

acts at α1-adrenoceptors on VSMCs to increase TPR –> increased BP
cardiac protective

108
Q

How’s NORAD cardiac protective?

A

No sig actions on heart (β1) so doesn’t make heart work hard to increase BP, blood flow

109
Q

Why’s Adrenaline given in high conc?

A

to have an action on both β1 on the heart and α1 on VSMCs to raise BP (also β2 in lungs to give bronchodilation)

110
Q

When do you increase vasodilation?

A

when hypertension is a risk factor in:

angina, HF

111
Q

Effects of hypertension?

A
  • causes endothelium dysfunction
  • reducing tonic vasodilatation processes (NO, PGI2)
  • poor end organ perfusion
  • increases afterload
  • poor CO
  • heart has to work much harder
112
Q

What causes raised BP?

A

Imbalance of vasoconstrictor + vasodilator mechanisms

Excessive vascular tone in arterioles suppling end organs

113
Q

Why does greater BP not mean greater drive?

A

greater pressure drop across arterioles since higher pressure upstream, lower pressure (lower blood flow) downstream of excessive constriction

114
Q

Diff vasoconstrictor mechanisms?

A
  • Stretch of receptors (myogenic response)
  • Activate vgcc
  • Increase membrane depolarisation
115
Q

Diff vasodilator mechanisms?

A

-Block receptors
-Open K+ channels hyperpolarisation
-Block vgcc
-Increase Ca ATPase SERCA:
more Ca into SR + more Ca exclusion from cell
-Decreased MLCK
-Increased MLCP (myosin light chain phosphatase)

116
Q

eg of Gq receptor blockers?

A

AT1 antagonist : ARB
ACE inhibitor
α1 antagonist
ETA1 antagonist

117
Q

Effect of ARB + eg?

A 
Block AT1 (Angiotension II) receptors to reduce vasoconstriction in hypertension, HF
Losartan
118
Q

Effect of ACE inhibitor + eg?

A

Reduce Ang II levels in hypertension, HF

Enalapril

119
Q

Effect of α1 antagonist + eg?

A

Competitive receptor antagonists – drug-resistance hypertension
Prazosin

120
Q

Effect of ETA1 antagonist + eg?

A

Block ETA receptors which are upregulated in pulmonary artery hypertension
Bosentan

121
Q

What type of drugs prevent increase in membrane excitability?

A

Nitrates

K channel openers

122
Q

How do drugs prevent increase in membrane excitability?

A

Hyperpolarisation

Inhibit VGCCs

123
Q

eg of Ca influx blockers?

A 
VGCC blockers (CCB)
K Channel Openers
124
Q

Effect of VGCC blockers (CCB) + eg?

A

Dihydropyridine subtype, vascular selective, block influx of Ca2+ to reduce vasoconstriction in hypertension, angina
Amlodipine

125
Q

Effect of K Channel Openers + eg?

A

Hyperpolarisation, less VGCC activation/Ca influx, vasodilatation for angina
Nicorandil

126
Q

eg of contractile mechanism relaxants?

A

Nitrates

PDE5 inhibitors

127
Q

Effect of nitrates + eg?

A 
NO donors, PKG-mediated vasorelaxations for angina, pulmonary oedema
Glyceryl trinitrate (GTN)
128
Q

Effect of PDE5 inhibitors + eg?

A

GMP breakdown, PKG-mediated vasodilatation for erectile dysfunction
Sildenafil

CVS II (19 decks)

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