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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
Ryanodine Receptor (RyR)
release spontaneous bursts of Calcium "sparks" * activates nearby Ca2+-dependent K+ channels which hyperpolarize the cell * does not cause contraction
26
Caveolae
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
27
Depolarizing the cell induces \_\_\_\_\_
vasoconstriction
28
Effect of Epinephrine on alpha receptors
vasoconstriction
29
Effect on Epinephrine on Beta-2
vasodilation
30
Effect of Histamine on H1 receptors
vasoconstriction
31
Myosin Light Chain Kinase (MLCK)
* phosphorylates the myosin light chains in the presence of ATP * cross bridge formation * smooth muscle contraction
32
"Latch State" of VSM
slow crossbridge cycling * maintains vascular tension * consumes less energy
33
Ion Movement in VSM
34
[Ca2+] cytosolic range in VSM
100-350 nM
35
Ca2+ Sequestration
Ca2+-ATPase pump in the SR that removes calcium out of the cytoplasm
36
Ca2+ Expulsion
Ca2+-ATPase pump in the sarcolemma that removes Calcium from the cytoplasm
37
anything that causes VSCC, ROC, or other cation channels to open results in \_\_\_\_\_
vasoconstriction
38
Explain hypoxia and the role of K channels
Hypoxia increases the fraction of open K channels, leading to hyperpolarization * closes voltage-sensitive Ca channels * reduces calcium infux * contributes to hypoxic vascular relaxation
39
What ion is unusually high in VSM?
chloride 54 intra -- 134 extra
40
Which Potassium channel senses ischemia and contributes to hypoxic vasodilation?
ATP-dependent K+
41
Which potassium channel senses extracellular potassium and contributes to vasodilation in exercising muscle, myocardium, and brain?
Inward-Rectifier K (Kir)
42
KATP-blocker drug
Glibenclamide * causes partial depolarization and vasoconstriction
43
KATP-activating drug
Nicorandil * causes vasodilation * nitrodilator used to treat angina
44
Which potassium channels contribute to resting potential and prevent vasospasm?
Voltage-dependent (Kv) and Ca-dependent (BK)
45
Which Calcium channel mediates depolarization-dependent contraction?
Voltage-Sensitive Ca2+ (VSCC)
46
Which calcium channel mediates depolarization-dependent contraction and contributes to agonist-induced electrical excitation?
Ca2+-conducting TRP
47
When potassium exits the VSM cell, the membrane potential becomes negative and as a result \_\_\_\_\_
less calcium enters the cell
48
Anything that opens a VSM potassium channel results \_\_\_\_\_
vasodilation
49
Agonism of Beta1 receptors result in \_\_\_\_\_
chronotropy, inotropy, lucitropy, and dromotropy.
50
Alpha-1 receptor agonist results in
vasoconstriction
51
Beta2 receptor agonism results in \_\_\_\_\_
vasodilation
52
Vasoconstrictor agonists examples
angiotensin II, vasopressin, serotonin, thromboxane, and endothelin
53
Alpha-1
* numerous in systemic blood vessels * NE \> Epi * activation leads to depolarization and vasoconstriction
54
Alpha-2
* numerous in cutaneous blood vessels * Epi \> NE * Decreases KATP conductance * depolarization and vasoconstriction
55
Beta-1
* found in cardiac pacemakers and myocardium * NE \> Epi * increase in heart rate and contractility * chronotropy and inotropy * cAMP pathway
56
Beta-2
* found in arterial vessels of myocardium, skeletal muscle, and liver * Epi \> NE * coupled to G-protein: cAMP * vasdilation
57
SR distribution
* 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
58
Fast Excitatory Junctional Potential (fast EJP)
* initial rapid depolarization * ATP mediated * binds to purinergic receptor (P2x) * conducts Na or Ca
59
Slow EJP
* triggered by norepinephrine * may or may not cause action potentials
60
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
61
Initial Phase of Contraction
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)
62
Phase 2 of Contraction
tonic phase * decrease in cytosolic [Ca2+] leading to partial depolarization * vasoconstriction maintained through calcium sensitization
63
Calcium Sensitization
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
64
Vasomotion
rhythmic contractions that help reduce the net capillary filtration rate
65
Four mechanisms of Vasodilation
* hyperpolarization * cAMP PKA * cGMP PKG * desensitization to calcium
66
Hyperpolarization mediated vasodilation
decreases opening of VSCCC leading to fall in free calcium and vasodilation * Examples * skeletal muscle contraction * sensory nerve neuropeptides * KATP-activating drugs
67
Vasodilation via Nitric Oxide
increases cGMP which activates protein kinase G * phosphorylation of phospholamban * decrease calcium sensitivity
68
Calcium Channel Blockers
bind to L-type calcium channels * smooth muscle relaxation * negative inotropy * affects phase 0 of pacemaker current * negative dromotropy
69
Therapeutic uses for CCB
* 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
70
(3) types of CCB
dihydropyridines, phenylalkylamine, and benzothiazepine
71
Dihydropyridines
vascular smooth muscle selective CCB * decrease SVR * powerful systemic vasodilators * "-pine"
72
Phenylalkylamine
CCB selective for myocardium * decreases myocardial oxygen demand * reverses coronary vasospasm * decreases HR * **Verapamil**
73
Benzothiazepine
CCB with intermediate selectivity * decrease inotropy * vasodilator * **Diltiazem**
74
vascular 'tone'
tension exerted by vascular smooth muscle * Determines * local blood flow * capillary recruitment and capillary pressure * arterial pressure * central venous pressure
75
Basal Tone
vascular tone of arterial vessels when the tonic sympathetic vasoconstrictor nerve activity is blocked
76
Extrinsic mechanisms for vascular control
controls the needs of entire organism * vasomotor nerves * circulating hormones * Epi, NE, angiotensin, vasopressin, insulin
77
Intrinsic regulatory mechanisms
* Bayliss myogenic response * endothelial secretions * vasoactive metabolites * autocoids * temperature
78
Responses mediated through Intrinsic mechanisms
* flow autoregulation * hyperaemia * inflammatory vasodilation * arterial vasospasm
79
Vascular Control Hierarchy
* 1st Tier (least) * myogenic response * autoregulation * 2nd Tier * intrinsic regulatory chemicals * vasodilators of metabolic hyperemia * 3rd Tier (most) * extrinsic regulation * vasomotor nerves and hormones
80
Bayliss Myogenic response
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
81
In what tissues does the myogenic response occur?
well developed in brain, kidney, and myocardium ## Footnote **Not in skin**
82
Mechanism of the Myogenic Response
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
What drugs block the myogenic response?
TRP-channel blocker (gadolinium), chloride channel blockers, ENaC blocker (amiloride), and CCB
84
What prevents excess myogenic constriction?
when a vessel narrows, the shear stress increases, stimulating the endothelium to produce more nitric oxide and EDHT
85
* when the myocyte is stretched, L-type calcium channels are activated causing contraction * wall tension maintains response
86
(3) Paracrine vasodilators produced by the endothelium
NO, EDHT, and PGI2
87
Roles of Nitric Oxide in vascular control
* 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
Nitrix Oxide and Basal vascular tone
* increased flow or viscosity increases the shear stress * produces NO causing vasodilation * increased insulin and estrogen * increase cardiac output, but decrease in MAP
89
Nitric Oxide and Inflammation
inflammatory autocoids (bradykinin, thrombin, and substance P) produce vasodilation by activating eNOS
90
Nitrate Drugs
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
Endothelin
vasoconstrictor produced by endothelium * activates calcium channels and increases cytosolic Ca2+ * vasoconstriction and venoconstriction lasts 2-3 hours
92
Pathological causes of increased endothelin production
* **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
Metabolic hyperaemia (functional hyperemia, metabolic vasodilation)
when the metabolic activity of an organ increases, the blood flow to the active region increases
94
Metabolic vasoactive factors
* acidosis * hypoxia * adenosine * potassium * phosphate * hyperosmolarity
95
Interstitial K role in metabolic hyperemia
released by active tissues due to repeated depolarization * increase extracellular [K+] * hyperpolarization causes less calcium entry through VSCC * vasodilation
96
Acidosis role in metabolic hyperemia
**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
Hypoxia role in metabolic hyperemia
**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
Adenosine role in metabolic hyperemia
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
Phosphate and Hyperosmolarity role in metabolic hyperemia
**vasodilation** * breakdown of ATP that causes an increase in [phosphate] and [K+]
100
hydrogen peroxide role in metabolic hyperemia
hyperpolarizing vasodilator * generated from breakdown of superoxide * increase as oxygen consumption increases
101
Autocoid regulation
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
Histamine
mediator of inflammation that is stored in mast cells and basophilic leukocytes * H1 receptor * increase vascular permeability on venules * H2 receptor * dilates arterioles
103
Bradykinin
produced during inflammaiton from kininogen * dilates resistance vessels * activation causes NO or EDHF production * increases venular permeability * produces pain
104
Serotonin (5HT)
made from AA tryptophan causing vasoconstriction, venular permeability, and pain * wide range of effects * produced in intestines, endothelium, CNS, and platelets
105
Prostaglandins and Thromboxane | (eicosanoids and prostanoids)
derivatives of AA that cause vasoconstriction * not inflammatory agents * steroids inhibit production of COX * NSAIDS are COX 1 and 2 inhibitors
106
Leukotrienes
mediators of the inflammatory response that increase vascular permeability ## Footnote Ex: bronchial inflammation of asthma
107
Platelet activating factor
produced during inflammation * promotes platelet aggregation * bronchoconstriction * vasospasm in coronary arteries * venular hyperpermeability
108
Metabolic Hyperemia
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
Where is autoregulation of blood flow not present?
pulmonary circulation
110
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
mechanisms of autoregulation
primarily by myogenic response * then vasodilator washout * increased pressure causes increased flow which "washes out" local vasodilator substances
112
Ascending vasodilation during exercise
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
Post-Ischemic Hyperemia
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
ischemia-reperfusion injury
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
Sympathetic nervous systemic activation in VSM
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
Preganglionic cholinergic fibers
activvate nicotinic receptors in sympathetic ganglia * travel through the ventral roots of the spinal nerves and white rami communicates * enters the sympathetic chains
117
postganglionic nonadrenergic fibers
innervate blood vessels * send non-myelinated axons through the grey rami communicates into the ventral roots * distribution in mixed periphral nerves
118
Neuromodulation
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
Pharmacology of alpha receptor
* vascular myocytes - vasoconstriction * NE \> Epi * antagonists * phentolamine and phnoxybenzamine * ergotamine * therapeutic uses * raynaud's vasospasm * acute hypertension * migraine
120
Pharmacology of Alpha-1 receptor
* post-junctional receptor on most vessels * vasoconstriction * NE \> Epi and phenylephrine * Antagonists * prazosin, doxazosin, and terazosin * Treatment * essential hypertension
121
Pharmacology of Alpha-2 receptor
* 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
Pharmacology of Beta receptors
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
Pharmacology of Beta-1
* SA node and myocardium * increase HR and contractility * NE \> Epi and dobutamine * Antagonists * atenolol, metroprolol, practolol * Treatment * angina, hypertension, and arrhythmias
124
Pharmacology of Beta-2 Receptors
* arterioles of heart, skeletal muscle, and liver * bronchial smooth muscle * dilation * Epi \> NE, Salbutamol, and terbutaline
125
Phenyleprine
alpha-1 agonist | (some alpha-2 and beta-1)
126
Clonidine
alpha-2 agonist | (some alpha-1)
127
Dexmedetomidine
alpha-2 agonist | (some alpha-1)
128
Epinephrine | (receptor)
alpha and beta agonist | (higher Beta-1)
129
Ephedrine | (receptor)
alpha-1 and beta-1 | (some beta-2)
130
Fenoldopam | (receptor)
DA-1
131
Norepinephrine | (receptor)
alpha and beta-1
132
Terbutaline | (receptor)
Beta-2 | (some beta-1)
133
Dobutamine | (receptor)
Beta-1 | (some beta-2)
134
Dopexamine | (receptor)
Beta-2 and DA-2 | (some DA-1)
135
Alpha-1 \>\>\>\> Alpha-2 antagonist
prazosin, terazosin, and doxazosin
136
Alpha-1 \> Alpha-2 Antagonist
phenoxybenzamine
137
Alpha antagonist example | (alpha-1 = alpha-2)
Phentolamine
138
Alpha Antagonist Example | (alpha-2 \>\> alpha-1)
Rauwolscine, yohimbine, and tolazoline
139
Mixed antagonists Beta-1 = Beta-2 \> alpha-1 \> alpha-2
labetaolol and carvedilol
140
Beta Antagonist Example | (beta-1 \>\>\> beta-2)
metoprolol, alprenolol, atenolol, esmolol
141
Beta Antagonist Example | (beta-1 = beta-2)
propranolol, timolol
142
Beta Antagonist Example | (beta-2 \>\>\> beta-1)
butoxamine
143
(3) main transmitters in sympathetic vasoconstrictors
norepinephrine, ATP, and Neuropeptide Y
144
(3) transmitters in parasympathetic dilators
ACh, VIP, and NO
145
(3) transmitters in sensory-dilator axons (C-fibers)
substance P, CGRP, and ATP
146
* Phentolamine (alpha-blocker) abolishes slow EJP
147
Neuropeptide Y (NPY)
* 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
Sympathetic fibers
* vasoconstrictors that are continuously active * reduced sympathetic output causes vasodilation * increased output raises peripheral resistance
149
Responses to increased sympathetic activity
* reduced local blood flow * decreased organ blood volume * capillary pressure decreases due to arteriolar constriction * total peripheral resistance increases
150
Mayer waves
oscilation of blood pressure due to cyclic changes in sympathetic vasomotor tone driven by a resonance in the baroreceptor reflex
151
Traube-Hering waves
oscillations in blood pressure during inspriation and exhalation
152
Parasympathetic System
* 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
Which tissues do not have a parasympathetic innervation?
skin and muscle
154
Neurotransmitters of PNS
* primarily **acetylcholine** * hyperpolarization and vasodilation due to NO production on intact endothelium * Non-adrenergic, non-cholinergic (NANC) * VIP, substance P, and NO
155
Sympathetic Vasodilator nerves
* ACh released * vasodilation is transient as there is a limited distribution of cholinergic fibers * primarily travels to sweat glands
156
Sympathetic Vasoconstrictor Fiber
* 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
Sympathetic Dilator Nerve
* Acetylcholine (and VIP) * distributed only in sweat glands * NOT tonically active * centrally controlled in forebrain * negligible baroreceptor reflex * unimportant in BP * transient duration
158
Lewis Triple Response
* 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
Dermatographia
extreme triple response where a simple touch leaves welts on the skin
160
Insulin
stimulates endothelium to produce NO * **vasodilator** * antithrombotic actions * inhibits vascular smooth muscle growth and migration
161
Thyroxine
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
Estrogen
vasodilator by activating NO synthase and BKCa channels
163
Relaxin
peptide hormone secreted during pregnancy * causes vasodilation in the uterus, mammary glands, and heart * attenuates endothelin-mediated vasoconstriction
164
Epinephrine
* 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
Norepinephrine
* increases BP and peripheral resistance * decreases HR and cardiac output ## Footnote alpha and beta effects, but alpha agonist predominates causing vasoconstriction
166
Vasopressin (ADH)
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
Angiontensin II
* stimulates aldosterole * promotes renal salt and water retention * vasoconstriction * raises peripheral resistance and BP * stimulates the thirst sensation
168
Atrial Natrituretic Peptide
* dilation of resistance vessels * increase sal and water excretion * fluid transfer from plasma to interstital compartment counteraccts the effects of the RAAS system
169
Structure of Adrenal Gland
* located on upper pole of kidney * outer: cortex * steroid hormones (cortisol and aldosterone) * inner: medulla * catecholamines
170
Triggers for Epinephrine secretion
exercise, hypotension, and hypoglycemia
171
Comparison of Epi and NE
172
Arterial pressure and HR in Epinephrine
173
Arterial pressure and HR in Norepinephrine
174
Vasopressin release
increased osmolarity and decreased blood pressure stimulates vasopressin release
175
Venous vs Arteriolar Control
* veins have little basal tone in the absence of sympathetic activity * do not have myogenic response * respond to hormones, autocoids, and drugs differently
176
Stimuli that activate RAAS
* hypotension * increased renal sympathetic activity * fall in NaCl concentration at the macula densa * reduced renal artery pressure
177
Coronary blood flow in resting human
70-80 ml/min/100g | (during heavy exercise, 300-400)
178
myocardial oxygen extraction at rest
65-75%
179
Oxygen Extraction
consumption/delivery
180
When does most coronary artery flow occur?
diastole
181
Main risk factors for coronary atheroma
* high LDL * hypertension * smoking * diabetes * obesity
182
Coronary artery structure increases likelihood of MI
functional end-arteries | (no anastomoses)
183
heart anatomy
184
Which coronary recieves a higher blood flow?
left
185
The primary method used by the coronary circulation to increase oxygen deliver is \_\_\_\_\_
vasodilation and increased blood flow
186
Unique considerations of Coronary perfusion
* O2 supply is flow limited * because extraction fraction is high at rest * functional end-arteries * prone to atheroma
187
Skeletal Muscle Circulation
* 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
Tonic (postural) Muscles
* blood flow at rest 15mL/min/100g * higher capillary density * 15% of all muscle fibers are red (slow)
189
Maximum flow to skeletal muscle can be \_\_\_\_\_\_
80-90%
190
Acral skin
high number of AVAs * fingers, toes, lips, nose, ears * little basal tone * lots of SNS innervation
191
Temperature Regulation
warmth receptors in anterior hypothalamus modulate SNS outflow to skin
192
Changes during Hyperthermia
core temperature \> 37.5oC * vasodilation and hyperemia * skin on limb and trunk increase sympathetic vasodilation * acral skin decreases SNS outflow leading to vasodilation
193
Hypovolemia
* 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
Cerebral Perfusion Pressure equation
MAP - ICP ## Footnote (if ICP \> CVP) MAP - CVP (if CVP \> ICP)
195
Average blood flowin cerebral circulation
55 mL/min/100g
196
Autoregulation of cerebral perfusion
* raised arterial CO2 causes vasodilation * low CO2 causes vasoconstriction * local sympathetic stimulation affects flow significantly only when arterial pressure is high
197
Cushing's Reflex
stimulation of vasomotor center in brainstem due to increased ICP * hypertension and reflex bradycardia
198
Cerebral Vasospasm
intracerebral hemorrhage * release endothelin, serotonin, and neuropeptide Y
199
Migraine
due to dilation of large extracerebral vessels * Treat with sumatriptan: 5HT-1 agonist * vasoconstriction
200
Regulation of Pulmonary Vascular Tone
* perfusion dependent on CO * no autoregulation * no metabolic hyperemia * autonomic NS innervation very small * HPV * primary influence over vascular tone
201
portal vein
70-80% of hepatic blood flow * yet contributes equally to O2 supply with hepatic artery
202
Intrinsic regulation of hepatic blood flow
* hepatic artery * autoregulation * metabolic hyperemia * hepatic portal vein * no autoregulation * in series with splanchnic vessels

Quarter 4 (15 decks)

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