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Cardio > Pharm Overview of CV Autonomic Nervous System > Flashcards

Pharm Overview of CV Autonomic Nervous System Flashcards

1
Q

α1 effect on CV

A

Vasoconstriction leading to increased BP

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2
Q

α2 effect on CV

A

Negative feedback - Can limit vasoconstriction by preventing further norepinephrine release from synapse

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3
Q

α1 mechanism

A

POSTSYNAPTIC, downstream signaling via DAG/IP3 leading to increased calcium

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4
Q

α2 mechanism

A

PRESYNAPTIC, “autoreceptors” that perform feedback inhibition of adenylate cyclase to decrease levels of cAMP

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5
Q

What receptors do epinephrine target? What is the effect on vessels?

A

Targets ALL alpha and beta receptors. Therefore, it creates a limited increase in blood pressure (vasoconstriction caused by alpha activation overcomes vasodilation from beta activation)

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6
Q

How do alpha-blockers affect epinephrine’s effects?

A

Allow only the vasodilatation effects due to epinephrine-stimulated beta-receptors to be seen, so you get a decrease in BP!

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7
Q

How do beta-blockers affect epinephrine’s effects?

A

Allow only the vasoconstriction effects due to epinephrine-stimulted alpha-receptors to be seen, so see further increase in blood pressure

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8
Q

What receptors do norepinephrine target? What is the effect on vessels?

A

Selectively targets alpha receptors (but can target beta1 receptors). Therefore, it creates an increase in BP due to vasoconstriction from alpha activation.

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9
Q

How do alpha-blockers affect norepinephrine’s effects?

A

Prevents vasoconstriction due to alpha activation and (since no beta effect really significant) does NOT cause vasodilation

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10
Q

How do beta-blockers affect norepinephrine’s effects?

A

Does NOT affect the vasoconstriction effects due to norepinephrine-stimulted alpha-receptors to be seen, so see no change in the increased blood pressure

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11
Q

Which alpha blockers are α1»>α2 ?

A

doxazosin, terazosin, and prozosin

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12
Q

Which alpha blockers are α1>α2 ?

A

phenoxybenzamine

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13
Q

Which alpha blockers are α1=α2 ?

A

phentolamine

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14
Q

Which alpha blocker has the longest half-life?

A

doxazosin

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15
Q

Which alpha blocker has the shortest half-life?

A

prozosin (take every 8 hours)

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16
Q

MOA of α1 specific blockers? 3 main pharmacological effects.

A

1) blocking the binding of norepinephrine to post-synaptic nerve endings (so you do NOT get vasoconstriction, leading to decreased peripheral resistance, which decreases BP)
2) Relieve symptoms of benign prostatic hyperplasia
3) Increase HDL, lower LDL

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17
Q

What is a consequence of starting alpha 1 blockers to control blood pressure?

A

Reflex tachycardia due to drop in blood pressure!

Orthostatic hypotension also occurs because you are blocking the alpha receptors (and vessels in legs cannot contract well to send blood back to brain)–worse with prazosin!

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18
Q

MOA of Nonspecific alpha-blockers?

A

Causes presynaptic α2-receptors to increase norepinephrine release (by blocking the negative feedback inhibition), resulting in increased cardiac output—which tempers the BP lowering action you get from α1 blockers.

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19
Q

Small doses of phentolamine have what affect on BP?

A

increase in BP (inotropic effect)

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20
Q

Large doses of phentolamine have what affect on BP?

A

decrease in BP (peripheral vasodilation)

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21
Q

Which is better for hypertension, diuretics or alpha blockers?

A

DIURETICS!

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22
Q

β receptor activity on heart?

A

Accelerates SA node, Accelerates ectopic pacemaker, Increase in contractility (beta1)

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23
Q

β receptor activity on vascular?

A

relaxes skeletal muscle vessels (beta2)

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24
Q

β receptor activity on kidney JG cells?

A

beta1 receptors stimulate renin release

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25
Q

Which beta-blockers are β1»>β2?

A

A-N “olols”

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26
Q

Which beta-blockers are β1=β2?

A

P-T “olols” and carteolol

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27
Q

MOA of beta-blockers on CV? Major pharmacological effects.

A

cardiac output falls, blood vessels constrict, lower HR, inhibition of renin release

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28
Q

Why do you want to use beta blockers with extended pharmacologic action? Which drugs?

A

you also get vasodilation so you get a larger drop in BP
carteolol, carvedilol, labetalol, betzxolol
(drugs that are not just “olol”)

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29
Q

What types of beta blockers can cause psychological effects (ex. vivid dreams)?

A

Drugs with High Lipid Solubility- Penbutolol, Propranolol

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30
Q

What is Intrinsic Sympathomimetic Activity?

A

partial agonist that binds to receptor (for a long time) and mimics stimulation of the SNS (so you are stimulating the heart at rest so you don’t get bradycardia) but will work to be an antagonist of the endogenous transmitter

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31
Q

What drugs have Intrinsic Sympathomimetic Activity?

A

pindolol, albutolol

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32
Q

What beta-blockers are membrane stabilizing?

A

Carvedilol, Albutolol, and Propranolol

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33
Q

Membrane stabilizing beta blockers are also called what?**

A

Known as Class 1 Anti-Arrhythmics because they bind to and block fast sodium channels causing a decrease in rapid depolarization.

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34
Q

What is the only beta-blocker given by IV infusion? Why?

A

Esmolol (because it has a very short half-life)

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35
Q

What affect to chronic NSIADs have on BP?

A

a 5 fold increase in BP despite of taking beta-blockers

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36
Q

Beta blockers work best on patients with what 3 conditions?

A

1) High-renin hypertension
2) Hypertensive patients with MI, IHD, or CHF
3) Hypertensive patients with hyperthyroidism and migraines

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37
Q

What are the adverse effects on beta-blockers on CV? Also stopping them?

A

CHF
Bradycardia (especially with calcium channel antagonists)
Cold extremities
Sudden angina and death if discontinue after long-term treatment (because you had upregulated receptors during treatment).

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38
Q

List the “off target” effects of beta-blockers?

A

LUNGS: non-selective beta blockers NOT for people with asthma or COPD (beta2 receptor antagonism for these people is BAD)

CNS- Depression, mental disorders, vivid dreams

GLUCOSE- hypoglycemia because beta2 stimulates hepatic glycogenolysis and pancreatic glucagon release

LIPID- beta receptors mediate lipolysis and beta blockers increase TGs and decrease HDLs

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39
Q

What is the “prevailing tone” in the heart?

A

parasympathetic! (want to negatively control heart so you don’t get tachycardia)

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40
Q

What is the “prevailing tone” in the vessels?

A

sympathetic! (don’t want blood pooling in the periphery)

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41
Q

What is the CV effect of acetylcholine? What receptors does it bind to?

A

neurotransmitter in sympathetic and parasympathetic ganglia that binds to cholinergic (GPCR) and nicotinic (ligand-gated ion channels) receptors on postganglionic emmbrane to maintain vascular tone and contraction.

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42
Q

MOA of Trimethaphan?

A

competitive antagonist of acetylcholine that blocks the binding site of the nicotinic receptor so that NO EPSP can form and NO ganglionic transmission can occur

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43
Q

What is bad about ganglionic blockers?

A

You have VERY LITTLE CONTROL of which ganglia are affected when giving a ganglionic blocker

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44
Q

What happens if alpha2 receptors are chronically stimulated?

A

inactivated by endocytosis.

45
Q

What is the MOA of clonidine?

A

Presynaptic autoreceptor that inhibits further release of catecholamine from pre-synaptic terminal to cause bradycardia and hypotension.

46
Q

Alpha 2 receptors must have what quality to work?

A

they must be able to cross the BBB

47
Q

List the alpha2 agonists? What is their ROA?

A

Clonidine- can be given IV, patch, or oral; very long lasting
Guanabenz- Oral
Guanfaline- Oral; longest halflife
Methyldopa- IV;shortest half-life

48
Q

What alpha2 agonists is a prodrug?

A

Methyldopa

49
Q

What drug should you prescribe with alpha2 receptors?

A

diuretics (because you get dependent salt and water retention)

50
Q

What is the most appropriate drug to treat a pregnant hypertensive woman?

A

Methyldopa

51
Q

What is the MOA of reserpine?

A

Binds tightly to target (adrenergic storage vesicles) in central and peripheral adrenergic neurons), inhibits VMAT2 (vesicular catecholamine transporter), and leads to a loss of capacity to concentrate and store NE and dopamine.

52
Q

Why do the effects of reserpine last so long?

A

The drug effects persist for days to weeks, because vesicles have to be reformed!

53
Q

What are some “off target” adverse effects of alpha2 agonists?

A
  • Somnolence (avoid with CNS depressants, give before bedtime)
  • Dry mouth (because alpha2 decreases salivary flow; may get more cavities!)
  • Abdominal pain, constipation, impotence
  • Hypotension, sinus bradycardia
54
Q

What are some CV adverse effects of alpha2 agonists?

A

a withdrawal of SNS tone producing fall in PVR and BP. This may lead to left ventricular hypertrophy!

55
Q

What is the MOA of reserpine?

A

sedation, increase suicidal ideation, TERATOGEN!

56
Q

What is reserpine?

A

deplete catecholamine stores by binding to storage vesicles in adrenergic neurons and destroying them so that neurons cannot aggregate or store NE or E.

57
Q

MOA of direct acting CV stimulants.

A

stimulate post-synaptic membrane

58
Q

MOA of indirect acting CV stimulants.

A

stimulate the heart by increasing the availability of NE via blocking metabolizing enzymes MAO or COMT or by blocking reuptake.

59
Q

MOA of mixed acting CV stimulants.

A

stimulate post-synaptic membrane AND release endogenous neurotransmitter from the presynaptic terminal

60
Q

Effect of reserpine on direct acting CV stimulants.

A

does NOT reduce CV stimulation (may actually increase it)

61
Q

Effect of reserpine on indirect acting CV stimulants.

A

completely abolishes response (because no NE to increase)

62
Q

Effect of reserpine on mixed acting CV stimulants.

A

blunts response but does not abolish it

63
Q

Mechanism of α1 downstream signaling.

A

Formation of IP3 and DAG, increase intracellular calcium

64
Q

Mechanism of α2 downstream signaling.

A

Inhibits adenylyl cyclase to decrease cAMP

65
Q

Mechanism of β1 downstream signaling.

A

stimulation of adenylyl cyclase and increase cAMP

66
Q

Mechanism of β2 downstream signaling.

A

stimulation of adenylyl cyclase and increase cAMP; activates cardiac Gi under some conditions

67
Q

Mechanism of D1 and D5 downstream signaling.

A

stimulation of adenylyl cyclase and increase cAMP

68
Q

Mechanism of D3 downstream signaling.

A

inhibition of adenylyl cyclase and increase in potassium conductance

69
Q

Effect of norepinephrine on pulse rate. Why?

A

decrease (due to baroreceptor reflex from the increase in peripheral resistance and resultant blood pressure)

70
Q

Effect of epinephrine on pulse rate. Why?

A

increase (due to beta1 receptor)

71
Q

Effect of Isoproterenol on pulse rate. Why?

A

increase (due to beta1 receptor)

72
Q

Effect of norepinephrine on blood pressure. Why?

A

increases in systolic and diastolic (increase in peripheral vascular resistance)

73
Q

Effect of epinephrine on blood pressure. Why?

A 
Increase systolic (alpha1)
Decrease diastolic (beta2)
74
Q

Effect of Isoproterenol on blood pressure. Why?

A 
Slightly increase systolic (due to increased CO)
Decrease diastolic (beta2)
75
Q

Effect of norepinephrine on peripheral resistance.

A

increase

76
Q

Effect of epinephrine and Isoproterenol on peripheral resistance. Why?

A

decrease (beta2 receptors in skeletal muscle vasodilate)

77
Q

The net effect of a drug is dependent on what 2 factors?

A

receptor selectivity + compensatory baroreceptor reflexes

78
Q

True or false: epinephrine can lower blood pressure.

A

TRUE: effects of epinephrine on the β2 receptor are stronger and more potent than those on α1, so at low does, epinephrine may actually cause a decrease in blood pressure.

79
Q

IV epinephrine delivery effects.

A

Increase in systolic blood pressure is greater than the decrease in diastolic blood pressure, so there is a net increase in blood pressure

80
Q

SC epinephrine delivery effects.

A

Local vasoconstrication at the injection site because of α1 effects leads the drug to have poor uptake (so acts like drug was given at low dosage). You get a predominant decrease in diastolic BP (with increase in heart contractility from beta receptors) and only a slight increase in systolic BP (due to compensatory response from increased heart rate.

81
Q

What is dopamine?

A

intermediate in the tyrosine→norepinephrine→ epinephrine pathway.

82
Q

How do you get around dopamine being impermeable to the BBB?

A

give it as a prodrug (carbidopa)

83
Q

What was dopamine historically used for?

A

maintaining renal perfusion by dilating renal vessels

84
Q

Describe the dose-dependent specificity of dopamine.

A

D1> β1 > α

85
Q

Low dose dopamine effects.

A

D1 effect on renal vasculature (dilation of vessels) and improve GFR

86
Q

High dose dopamine effects.

A

activates D1 and β1 to increase CO (contractility>HR) but also has vasodilation

87
Q

Very high dose dopamine effects.

A

activates α receptors to increase resistance and lead to renal vasoconstriction.

88
Q

What receptors does Phenylephrine affect?

A

alpha receptors only

89
Q

What is the effect of Phenylephrine?

A

potent vasoconstriciton and decreased HR and CO as a compensatory baroreceptor reflex.

90
Q

What is the ROA of Phenylephrine?

A

IM, IV, and SC

91
Q

What is Phenylephrine used for?

A

is used to control hypotension (including hypotension induced from anesthesia)

92
Q

What are the adverse effects of Phenylephrine?

A

very lipophillic so can cause CNS problems

93
Q

What receptors does Ephedrine affect?

A

alpha and beta

94
Q

What is the effect of Ephedrine?

A

works as a cardiostimulant that also increases BP.

95
Q

What is the ROA of ephedrine?

A

oral (seen in OTC cold medications)

96
Q

Why do you use ephedrine? What is its adverse effect?

A

used to treat hypotension but can lead to angina, palpitations, and arrhythmias

97
Q

What is interesting about OTC ephedrine?

A

can be used to make meth

98
Q

Effect of Ach on M2 receptor.

A

slows SA node activity (decrease HR), slows AV node conduction velocity, decrease atrial contractility, NO REAL EFFECT on ventricle

99
Q

How does the M2 receptor pathway work?

A

• Couples by Gi/Go pathway to decrease adenylate cyclase and decrease cAMP levels.
• This leads to hyperpolarization of membranes
o Stimulates K-Ach channels (inward rectifying)
o Inhibits voltage gated, L-type calcium channels

100
Q

Effect of Ach on M3/M5 receptor.

A

effects vasculature by synthesis and release of EDRF (vasodilating intermediate)

101
Q

How does the M3 receptor pathway work?

A

• Gq coupling pathway to increase IP3 and DAG which increases Calcium and PKC
o Leads to depolarization (excitation) of membrane
o Increases synthesis and release of NO (vasodilation)

102
Q

How does the M3 receptor pathway work if endothelial injury has occurred?

A

if endothelial injury occurs, Ach will bind directly to M3 receptors in vascular smooth muscle leading to vasoconstriction.

103
Q

Explain the interplay between adrenergic and cholinergic control of the heart.

A

Adrenergic (sympathetic) and cholinergic (parasympathetic) nervous control of the heart are controlled by both autoreceptors (feedback inhibition of their own release) AND heteroreceptors (inhibition of the OTHER system’s neurotransmitter release).

104
Q

Effect of low dose atropene.

A

inhibits M1 autoreceptors and increases Ach release to decrease HR.

105
Q

Effect of high dose atropene.

A

blocks M2 on SA nodal cells to increase resting HR (inhibits vagal tone)

106
Q

Does atropene effect the vasculature?

A

Not usually, , but at high enough doses, it can dilate cutaneous blood vessels (as a compensatory reaction, because sweating is inhibited and body builds up heat that must be released) and lead to an “atropine flush.”

107
Q

Why would you administer atropene?

A

1) Counteracts the peripheral vasodilation and fall in BP caused by choline esters.
2) Abolishes reflex vagal cardiac slowing or asystole
3) facilitates AV conduction in patients with inferior/posterior MI by relieving sinus/nodal bradycardia or AV block

108
Q

Do beta blockers have to be administered with a diuretic?

A

NO, but if they are, the effect is additive.

109
Q

List the off-label uses of beta blockers.

A

Stage Fright

Altering memories

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