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4. Physiology and pathophysiology > Autonomic system > Flashcards

Autonomic system Flashcards

1
Q

B adrenergic R in heart

A

B1 > B2 subtype

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2
Q

Types of B adrenergic R and effects

A

o B1-R subtype: concentration => SA node (7x) > ventricles > atrial + AV node

o B2 R subtype: non cardiac = bronchodilation
 Inotropic + lusitropic effects from terminal neurons of cardiac ∑ nerves (NE release)
o B3 R subtype: adipose tissue > heart
 Mediate breakdown of fat
 Negative inotropic effect: might contribute to poor fct in CHF

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3
Q

Intracell signaling B-R

A

o Adrenergic stim → release Epi (adrenal gland) + NE (nerve terminal) → β-R
o G protein coupled R => bind to GTP prot => activate (Gs) adenylyl cyclase => incr cAMP → activate PKA => intra¢ signals

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4
Q

Effects of B stim on heart

A

+ inotrope
+ lusitrope
+ chronotrope
+ dromotrope

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5
Q

MOA + inotrope effect of B-R stim

A

incr rate of contraction + force developed
 PKA → Pi L-type Ca2+ channels → incr Ca2+ entry through ¢ membrane => incr Ca2+ induced Ca2+ release from RyR=> incr intra¢ Ca2+
* incr Myosin ATPase activity => incr rate of development of contractile force
* incr Ca2+ interaction w TnC => incr force developed
* Calmodulin activation => incr PDE activity => incr cAMP breakdown

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6
Q

MOA + lusitrope effect of B-R stim

A

 Phospholamban-Pi on SR + incr [Ca2+] => incr activity of Ca2+ pump
 TnI-Pi by PKA => incr rate of crossbridge detachment

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7
Q

MOA + chornotrope effect of B-R stim

A

 PM stimulation (SA node)

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8
Q

MOA + dromotrope effect of B-R stim

A

 incr conduction velocity down AV node => short PR
* Slow Ca2+ channel stimulation
 incr conduction velocity down His bundle, Purkinje fibers

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9
Q

Explain feedback mechanism after B-R stim

A

o Desensitization: physiological decr response w/i minutes
 Uncoupling: Sustained stimulation => B agonist R kinase (B ARK) => Pi of COOH tail of R => uncouples from Gs prot and ↑ affinity for arrestin → configuration change
* B ARK expression/activity: major regulator of cardiac contractile function
o Long term B stimulation => incr mRNA expression for B ARK
o Long term B blockade => decr B ARK
 Desensitization also accentuated by Pi of β-R by PKA
* Prevent adverse effects of intracell ↑cAMP
o Internalization: long term inhibitory mechanism: prolonged desensitization B R sequestration and internalization
 Can participate in growth signaling => formation of complex
* B-R/arrestin/tyrosine kinase
* Arrestin change molecular conformation of R
 Reversible: resensitization → phosphatase release P group => R can be linked to G prot again
o Digestion: via intracell proteolytic enzymes
 Irreversible

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10
Q

Effects of dobutamine on B adrenergic response

A

B1 R agonist => drug tolerance by desensitization + R downregulation

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11
Q

Effect of B blockers on B adrenergic response

A

o B blockers (atenolol, propanolol) => may be beneficial for decr B ARK expression → improve β adrenergic signaling

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12
Q

Effect of A stim on CV syst

A
  • Substantial vascular effects → vasoconstriction → ↑ PVR and BP
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13
Q

Intracell signaling of A-R stim

A

o Release of NE (vascular nerve terminal) => bind to A-R (G protein) => activate adenylyl cyclase => incr cAMP => PKC => IP3 + DAG => incr cytosolic Ca2+
 IP3 = phosphatidyl inositol system
* Stimulates release of Ca2+ from SR
 DAG = diacyglycerase
* Lipophilic => stays in ¢ membrane => activate PKC
* Sustained vasoconstriction

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14
Q

Cardiac effects of A-R stim

A

o Small positive inotrope via post synaptic A1-R =
> IP3 => icnr Ca2+
 Not major impact in normal myocardium
 May have an effect in CHF: downregulation of B adrenergic response

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15
Q

Types of A adrenergic R

A

o Post synaptic A1-R: inhibited by prazosin
o Presynaptic A2-R: inhibited by Yohimbine
o Other R coupled to phospholipase C: Ang II-R

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16
Q

Intracell signaling of muscarinic/cholinergic R

A
  • Ach (NT) => G protein coupled R => bind to GTP prot => inhibit (Gi) adenylyl cyclase => decr cAMP
    o cGMP = opposite effects vs cAMP
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17
Q

Parasymp R types in heart

A

M2 > M3 (NO linked R on endothelium)

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18
Q

Types of parasymp cholinergic R

A

 Nicotinic R: autonomic ganglia
* Respond to nicotine
* Inhibited by ganglion blocking agents (hexamethonium)

 Muscarinic: in tissues
* Inhibited by atropine
* M2: associated w vagal nerve activity  negative inotrope

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19
Q

Cardiac effects of cholinergic stim

A

Bradycardia
neg inotrope
neg dromotrope

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20
Q

MOA negative chronotrope effect of Ach

A

 G dependent K+ channel opening => inhibit rate of spontaneous depol => slow SA node
 Negative Treppe effect mediated by NO => decr HR
 Ach directly inhibits SA node

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21
Q

MOA negative inotrope effect of Ach

A

 Ventricles < atrial response to muscarinic agonists despite similar R density
* Shorten atrial AP
 NO => activate guanylyl cyclase => incr cGMP => negative inotrope
* Also inhibit cAMP production

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22
Q

MOA negative dromotrope effect of Ach

A

 Gi → inhibit conduction through AV node

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23
Q

Role of NO in psymp effect on heart

A
  • NO may contribute to icnr inhibitory cGMP + incr Ach release
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24
Q

How is NO released and effect

A

Release by endothelial ¢ from incr blood flow/shear stress => diffuse in vascular smooth muscle ¢ => stimulate cGMP => incr cytosolic Ca2+ => vasodilation

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25
Q

Role of insulin and IGF

A
  • Regulates ¢ growth
  • Act on tyrosine kinase => signaling system that activates nuclear transcription => promotes growth
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26
Q

Effects of incr cAMP

A

Organelles influences by cAMP
* Activation of PK => Pi of
o Sarcolemmal prot of Ca2+ channel
o Phospholamban on SR
o TnI => Pi of inhibitory subunit = decr sensitivity to Ca2+ + promotes crossbridge detachment => incr relaxation
* PK: 2 subunits => regulatory or catalytic
o PK activity ratio proportional to cAMP levels
o PKA : predominates in cardiac ¢
o PKC: in response to A adrenergic, ET-I, Ang II

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27
Q

Other agents that incr cAMP

A

Glucagon
T3
Adenosine
PGI
Dopamine
PDEi
Histamine

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28
Q

MOA glucagon effect ion heart

A

hypoglycemia => incr glucagon secretion from pancreas => incr cAMP in liver ¢ => incr glycogen breakdown
o incrHR + contractility

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29
Q

MOA thyroxine effect on heart

A

Bind to nuclear R => stimulate variety of RNA formation => activate adenylyl cyclase

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30
Q

MOA adenosine effect on heart

A

formed by breakdown of ATP => couples to Gi
o Open K+ channel (IK-Ach) => hyperpolarization => inhibit Ca2+ entry → decr HR
o ↓ contractility from ↓ Ca2+
o Regulate apoptosis and protect from reperfusion injury

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31
Q

MOA prostacyclin effect on heart

A

PG released by vascular endothelium => Gs => activate AC => incr cAMP

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32
Q

MOA dopamine effect on heart

A

catecholamine NT => stimulate pre/post dopamine R
o Low [dopamine] → peripheral DA1-R → vascular SM relaxation → vasodilation
o High [dopamine] → central DA-R → ↑ NE release in nerve ending → activate β1-R → incr contractility
o ↑↑↑ High [dopamine] → cross reaction w/ α1-R → vasoconstriction

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33
Q

MOA PDEi effect on heart

A

inhibit cAMP breakdown => incr contractility, rate of relaxation, HR

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34
Q

MOA histamine effect on heart

A

H2 => coupled to AC => incr cAMP

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35
Q

Effect of CHF on autonomic system

A
  • decr myocardial fct => hypotension => stimulate baroR => symp activation
    o B mediated tachycardia
    o A mediated vasoconstriction
  • Receptors: decr # of B1-R, more prominent B2-R
    o decr inotropic response to catecholamines
     Negative inotropic effect of β3-R
    o Inhibit formation of cAMP via Gi signaling
  • incr plasma [NE]: degree of inrc proportional to severity of HF => related to px

B1-R downregulation
* Chronic/high exposure to catecholamines => decr myocardial responsiveness = desensitization
o B adrenergic R kinase => Pi-B1-R => inactivation
* Role of B2-R: become more prominent as B1-R # decr
o Not full expected inotropic result
o May be linked to Gi protein => negative inotropic antiapoptotic effect

36
Q

B adrenergic blockers in HF

A
  • Anti-arrhythmic effects
  • Reverse remodelling
  • Improve internal Ca2+ cycling
    o Inhibit hyperphosphorylation of RyR => decr excessive release of Ca2+ and Ca2+ overload
  • decr uptake/use of free fatty acids
37
Q

Types of R

A
  • G protein coupled R: GTP binding prot → Gi or Gs
  • Ion channel linked R: open channel when bind to ligand
  • Direct binding of intracell targets: bind to guanylyl cyclase
  • Enzyme linked R: enzyme/kinase activated when bond to ligand
    o Tyrosine kinase R
    o Sernine/threonine kinase R
    o Receptor guanyly cyclase
    o Phosphatases
  • Nuclear R: bind to hormones
    o Thyroxine, aldosterone
38
Q

G protein coupled R: structure, activation

A

o Major type in cardiovascular system
o G-prot have 3 subunits: Gα, Gβ, Ggamma
 Gαs → activate adenylyl cyclase → ↑cAMP
 Gαi → inhibit adenylyl cyclase → ↓cAMP
 Gαo → open K+ channels
 Gαq → activate PLC cascades
 Gβgamma → can activatite PLA, PLC, IK-Ach
o Activation: ligand bind to R → activation of Gα
 Gα-GTP dissociate from Gβ → intracell targets
 Intrinsic GTPase → Gα-GDP → bind to Gβgamma → reform basal state of R

39
Q

Intracell 2nd messenger

A

cAMP
cGMP
IP3 and DAG
NO

40
Q

Effect of cAMP

A

o Mediates most cardio response to ∑ stimulation
o Gαs → adenylyl cyclase → cAMP → cAMP dependent prot kin
o Gαi → inhibits cAMP formation
o cAMP degradation by PDE

41
Q

Role of cGMP

A

o Opposite actions to cAMP (couterregulatory)
o Respond to NO and natriuretic peptides → guanylyl cyclase → cGMP → cGMP dependent prot kin
o cGMP degradation by PDE

42
Q

Role of IP3 and DAG

A

o Synthetized from PIP2 in cell membrane → phospholipase C
o IP3: release Ca2+ from IP3 gated Ca2+ release channels → ↑ intracell [Ca2+] → vascular SMcell vasoconstriction (no effect on contractility)
o DAG: weak effect on contractility

43
Q

Role of NO

A

o L-arginine via nitric oxide synthase (NOS)
o NO bind guanylyl cyclase → ↑cGMP
o Rapid degradation

44
Q

Signaling enzymes

A
  • Protein kinases
    o Transfer Pi from ATP
    o PKA: cAMP activated
    o PKG: cGMP activated
    o PKC: phospholipid activated
    o CAM: Ca2+ activated
45
Q

Vasomotor center receives signals from

A

autonomic control of circulation => receives signals from baroreflexes => transmit impulses to vasodilator/constrictor fibers to arterioles

46
Q

Areas of vasomotor center

A

o Located in reticular substance of the medulla and lower pons: areas
 Vasoconstrictor area: continuously transmit signals => symp tone
 Vasodilator area: inhibit vasoconstrictor area
 Sensory area: nucleus solitarius
* Terminal site of afferent stimuli
o From baroR in response to incr or decr pressure
o Glossopharyngeal and vagal nerves
o Reflex activation of vasodilator/constrictor area
* BaroR => vagus/glossopharyngeal nerve => adrenergic/cholinergic vagal systems

47
Q

Structure of symp system innervation

A

o Symp fibers leave spinal chord through thoracic spinal nerves + 1-2 lumbar
 symp chain on each side of vertebral column => enter circulation (all vessels except capillaries)
 Adrenal medulla => NE/Epi release

48
Q

origin of vagus nerve

A

Vasomotor center

49
Q

Control of vasomotor center

A

o Control by higher centers: can be inhibited/stimulated
 Neurons in reticular substance of pons, mesencephalon, diencephalon
* Excitation: lateral + superior portions of reticular substance
* Inhibition: medial + inferior portions
 Hypothalamus
* Excitation: posterolateral portions
* Inhibition: anterior portions
 Cerebral cortex

50
Q

Effects of Epi/catecho infusion

A

 incrHR + systolic BP
 decr diastolic BP => stable mean BP
* Stimulates vascular vasodilatory B2-R
* Presynaptic R => promote NE release
 2 majors effects: incr CO + incr limb blood flow

o Vascular A-R vasoconstriction tend to offset B-R vasodilation

51
Q

Effects of NE

A

 incr HR + systolic + diastolic BP
* incr CO but decr limb blood flow

52
Q

Difference in effects of Epi vs NE

A

NE stimulates both vascular A-R and cardiac B-R
* incr HR is transient => will decr 2nd to baroR response to vasoconstriction

53
Q

Formation of NE

A

 Formed by dopa + dopamine + tyrosine (A.A)
* Released from terminal varicosities
* Some interact w R, some go into circulation
o Stimulate post synaptic A1-R = vasoconstriction
o Stimulate pre synaptic A2-R = feedback inhibition of its own release

54
Q

Neuromodulators of NE

A
  • Ang II => incr NE release
  • Adenosine + NO + incr psymp => decr NE release
55
Q

Effects of cholinergic system

A

o Inhibit NE release => vasodilation
o NO release from endothelial ¢ (if normal)
o Adenosine: vasodilatory local mediator

56
Q

Baroreflexes influencing psymp and symp syst activation

A

BaroR
Low P R
Brainbridge
Chemo R
CNS ischemic response
Cushing reflex
Abd compression reflex
Contraction of skeletal muscles

57
Q

Location baroR

A

carotid sinus + Ao arch on arterial side of circulation

58
Q

Role baroR

A

o 1st defense line against acute hypo/hypertension

o Short term regulation of BP
 Rapid response to acute BP variation
 Maintain BP in normal range during normal daily activity
 Not importance in chronic regulation: will reset to new “normal” BP

59
Q

Trigger of baroR

A

o Stretch R: respond to arterial distension (rather than P)
 Rate of pressure induced, stretch mediated deformation, sustained BP changes

60
Q

MOA baroR hypertension

A

 Hypertension: incr signals => vasomotor center => vagal nucleus => incr psymp outflow, incr vagal tone => decr HR, contractility => decr CO => decr BP
* Carotid sinus massage = induce same response

61
Q

MOA baroR hypotension

A

 Hypotension: decr signal frequency => vasomotor center => incr symp outflow, decr vagal
* B mediated response: incr HR + contractility => incr CO
* A mediated vasoconstriction => incr PVR => incr BP

62
Q

Location of low P R

A

cardiopulmonary R on venous side of circulation

63
Q

Trigger of low P R

A

o Stretch R in atria, PAs, ventricular endocardium => response to volume overload

64
Q

MOA low P R

A

Respond to alterations of filling volumes on venous side of heart
 icnr blood volume => incr signals from vagal afferent fibers => brain => decr symp outflow, decr renin release

65
Q

Brainbridge reflex

A

o Stretch R at jct of LA and PVs => directly activate SA node
o incr atrial pressure => incr HR/contractility
 Mediated by vagus afferent, symp efferent

66
Q

Chemo R MOA

A

o Chemosensitive ¢: decr O2, incr CO2/H+
o Respond to decr BP => excite vagus nerves => vasomotor center
 Not much activity in normal pressure range
o Important role in control of respiration

67
Q

MOA CNS ischemic response

A

2nd to incr CO2
o Ischemia of vasomotor center => incr stimulation of vasoconstrictor center => incr BP

68
Q

Cushings reaction MOA

A

incr pressure of CSF around brain => incr BP

69
Q

Abdominal compression reflex

A

initiation of baroR or chemoR => impulse to abdominal organs => tensing of abdominal muscles => incr blood return to heart

70
Q

Acute control of PVR

A

Local tissue control: blood flow according to metabolic demands

Low P reflexes

high pressure reflexes

Local messenger

71
Q

What local tissue control incr tissue blood flow

A

 Vasodilator theory: stimulate adenosine release +/- other vasodilators
 O2 demand theory: O2 needed for vasoconstriction
* decr O2 availability => vasodilation
 Other nutrients deficiencies => vasodilation
* decr glucose
* decr A.A or fatty acids
* decr Thiamine, niacin, riboflavin

71
Q

Autoregulation of blood flow

A

blood flow will return to normal after BP changes
 Metabolic theory: incr arterial pressure => incr nutrient delivery => incr vasoconstriction
 Myogenic theory: reflex constriction 2nd to wall stretch
 Tubuloglomerular feedback:
* Composition of fluid in early distal tubule => macula densa
* If incr fluid filtered => signals => vasoconstriction of afferent arteriole => decr renal blood flow and GFR
 Brain: excess CO2 => vasodilation

72
Q

Low pressure reflexes for PVR regulation

A

o Stimulation of renin release by => renal artery pressure
o A1 mediated vasoconstriction by baroreflex activation
o B1 mediated response

73
Q

Low pressure reflexes for PVR regulation

A

o decr symp outflow => decr renin release => decr angiotensin mediated vasoconstriction
o Endothelial regulation of BP (local messengers)
 Normal endothelium: incr shear forces => release of NO
 Diseased: ET-1 release

74
Q

Local messenger influencing PVR

A

o Endothelial NO
 NO is a gas, free radical that acts only locally where it is formed
 Synthetized in normal vascular endothelium, nerve terminals of NO releasing nerves
* Released 2nd to shear stress, incr blood flow
 Actions
* Inhibit symp outflow
* decr NE release
* incr relapse of Ach

o Adenosine: formed from ATP breakdown
 incr when rate of breakdown > resynthesis (ie. exercise)
 Actions
* Adenosine R on vascular SM¢ => direct vasodilation
* Neuromodulator => decr NE release
o Endothelin: vasoconstrictor
 Released by damaged endothelium

75
Q

Long term control of PVR

A
  • incr vascularity of tissues
    o Vascular remodeling
    o incr # of vessels => incr in O2 deprivation
  • Growth of new vessels: 4 factors
    o Vascular endothelial growth factor
    o Fibroblast growth factor
    o Platelet derived growth factor
    o Angiogenin
    o Inhibitors: angiostatin, endostatin, steroids
  • Collateral circulation
76
Q

Humoral regulation of PVR: vasoconstrictors

A
  • NE/epi: released from adrenal medulla + NE from symp nerve terminal
  • Angiotensin
  • Vasopressin: incr H2O reabsorption from renal tubules + powerful vasoconstrictor
    o Produced by hypothalamus
    o Stored in posterior pituitary
77
Q

Humoral regulation of PVR: vasodilators

A
  • Bradykinin
    o A2-macroglobulin => protease (kallikrein) released from tissues split into kallidin => form bradykinin
     Powerful vasodilation
     incr vascular permeability
  • Histamine
    o Released from basophils in blood/mast ¢ in tissues
     Vasodilation
     incr vascular permeability
78
Q

Effect of ions on PVR

A
  • incr Ca2+ => vasoconstriction
  • incr K+, Mg2+, H+ => vasodilation
  • Anions (citrate, acetate) => mild vasodilation
  • incr CO2 => vasodilation in brain
79
Q

Psymp system organization

A
  • Medulla oblongata: vagal nuclei => nerves from originate from cranial and sacral locations => preganglionic fibers => cardiac branches of vagal nerve => synapse in heart w ganglionic neurons
    o Post ganglionic neurons distributed to atria and to a lesser degree to ventricles
80
Q

Effect of vagal stimulation

A

NO release => Ach release
 Ach bind M2 R => activate Gi => inhibit cAMP prod
* decr Pi of L type Ca2+ channels
* Activates IKACh => hyperpolarize ¢
* Negative dromotropic and chronotropic

81
Q

Effect of vagal tone on SA node

A

o Autonomic tone have > influence on SA node because of denser innervation

fibers from ganglia in PV fat pad (btw CrVC and CaVC, adjacent to RPV)
 More affected by R vagal nerve
 decr rate of SA nodal d/c => decr rate of diastolic depol
* Inhibit effects of adrenergic stimulation: decr probability of opening If and ICa-L

82
Q

Effect of vagal tone on AV node

A

fibers from ganglia in fat pad at entry of coronary sinus into caudal interatrial septum, at jct of CaVC and caudal LA
 More affected by L vagal nerve
 Slow AV nodal conduction => inhibitory stimuli
* Stimulation/inhibition of L type Ca2+ current

83
Q

Effect of vagal tone on atrial myocytes

A

decr contractility by shortening AP and refractory period (activation of IKAch)
o decr probability of channel opening in plateau phase
o decr Ca2+ levels contibuting to decr contractility

84
Q

Effect of vagal tone on ventricular myocytes

A

intramural/subendocardial fibers => rise to epicardium in AV groove => very little supply to ventricles
o decr ventricular contractility by decr cAMP production

85
Q

MOA vagal maneuver

A

Stimulation of carotid BaroR => stimulates nerve of Hering (branch of 9th cranial nerve) => afferent impulse to vasomotor center => vagus nerve stimulation => decr SA node d/c and AV node conduction

86
Q

MOA atropine response test

A

Oppose vagal stimulation: block Ach binding sites

4. Physiology and pathophysiology (18 decks)

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